21 results on '"Verstuyf, Annemieke"'
Search Results
2. List of Contributors
- Author
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Adams, John S., primary, Adams, Judith E., additional, Alsalem, Jawaher A., additional, Anderson, Paul H., additional, Andreopoulou, Panagiota, additional, Angellotti, Edith, additional, Arnold, Leggy A., additional, Atkins, Gerald J., additional, Barbáchano, Antonio, additional, Bassuk, Shari S., additional, Beaudin, Sarah, additional, Belorusova, Anna Y., additional, Benkusky, Nancy A., additional, Bernal-Mizrachi, Carlos, additional, Bhan, Ishir, additional, Bhattoa, Harjit P., additional, Bikle, Daniel D., additional, Bilezikian, John P., additional, Binkley, Neil C., additional, Bischoff-Ferrari, Heike A., additional, Bishop, Charles W., additional, Boisen, Ida M., additional, Bonelli, Fabrizio, additional, Boskey, Adele L., additional, Boucher, Barbara J., additional, Bouillon, Roger, additional, Bouttier, Manuella, additional, Boyan, Barbara D., additional, Bruce, Danny, additional, Buburuzan, Laura, additional, Burghardt, Andrew J., additional, Burne, Thomas H.J., additional, Calvo, Mona S., additional, Camargo Jr., Carlos A., additional, Cannata-Andia, Jorge B., additional, Cantorna, Margherita T., additional, Carlberg, Carsten, additional, Carmeliet, Geert, additional, Carpenter, Thomas O., additional, Carter, Graham D., additional, Cashman, Kevin D., additional, Ceglia, Lisa, additional, Christakos, Sylvia, additional, Christopher, Kenneth B., additional, Chun, Rene F., additional, Coe, Fredric L., additional, Coffman, Frederick, additional, Compston, Juliet, additional, Cooper, Cyrus, additional, Curtis, Elizabeth M., additional, Cusano, Natalie E., additional, Danilenko, Michael, additional, David Roodman, G., additional, Dawson-Hughes, Bess, additional, De Clercq, Pierre, additional, DeLuca, Hector F., additional, Demaret, Julie, additional, Demay, Marie B., additional, Dempster, David W., additional, Dennison, Elaine M., additional, Dhawan, Puneet, additional, Dimitrov, Vassil, additional, Dixon, Katie M., additional, Doroudi, Maryam, additional, Doyle, Shevaun M., additional, Dusso, Adriana S., additional, Dvorzhinskiy, Aleksey, additional, Ebeling, Peter R., additional, Eisman, John A., additional, Emkey, Gregory R., additional, Epstein Jr., Ervin H., additional, Epstein, Sol, additional, Eyles, Darryl, additional, Favus, Murray J., additional, Feldman, David, additional, Ferrer-Mayorga, Gemma, additional, Findlay, David M., additional, Fleet, James C., additional, Foster, Brian L., additional, Franceschi, Renny T., additional, Fraser, David R., additional, Furst, Jessica M., additional, Gafni, Rachel I., additional, Giovannucci, Edward, additional, Girgis, Christian M., additional, Gleason, James L., additional, Glorieux, Francis H., additional, Gocek, Elzbieta, additional, Goltzman, David, additional, González-Sancho, José Manuel, additional, Graeff-Armas, Laura A., additional, Grant, William B., additional, Groves, Natalie J., additional, Gysemans, Conny, additional, Hansen, Lasse Bøllehuus, additional, Harvey, Nicholas C., additional, Hawrylowicz, Catherine M., additional, Hayes, Colleen E., additional, Heaney, Robert P., additional, Hendy, Geoffrey N., additional, Hershberger, Pamela A., additional, Hewison, Martin, additional, Holick, Michael F., additional, Hollis, Bruce W., additional, Hujoel, Philippe P., additional, Hyppönen, Elina, additional, Insogna, Karl L., additional, Jablonski, Nina G., additional, Jensen, Martin Blomberg, additional, Jolliffe, David A., additional, Jones, Glenville, additional, Jones, Kerry S., additional, Jüppner, Harald, additional, Kallay, Enikö, additional, Karaplis, Andrew C., additional, Kaufmann, Martin, additional, Kiely, Mairead, additional, Kim, Tiffany Y., additional, Konrad, Martin, additional, Kovacs, Christopher S., additional, Kremer, Richard, additional, Krug, Roland, additional, Kumar, Rajiv, additional, Kurihara, Noriyoshi, additional, Laing, Emma, additional, Lane, Joseph M., additional, Larner, Dean P., additional, Larriba, María Jesús, additional, Laverny, Gilles, additional, Le Roy, Nathalie, additional, Lee, Seong M., additional, Levine, Michael A., additional, Lewis, Richard, additional, Lips, Paul, additional, Lisse, Thomas S., additional, Liu, Eva S., additional, Liu, Philip T., additional, Li, Yan, additional, Li, Yan Chun, additional, MacKrell, James G., additional, Mady, Leila J., additional, Majumdar, Sharmila, additional, Makishima, Makoto, additional, Malloy, Peter J., additional, Mann, Elizabeth H., additional, Manson, JoAnn E., additional, Martineau, Adrian R., additional, Mason, Rebecca S., additional, Mathieu, Chantal, additional, Matsumoto, Toshio, additional, Matthews, Donald G., additional, McGrath, John J., additional, Metzger, Daniel, additional, Meyer, Mark B., additional, Miao, Denshun, additional, Mizwicki, Mathew T., additional, Moon, Rebecca J., additional, Morris, Howard A., additional, Mortensen, Li J., additional, Muñoz, Alberto, additional, Nakamichi, Yuko, additional, Narvaez, Carmen J., additional, Nashold, Faye E., additional, Naveh-Many, Tally, additional, Nielson, Carrie M., additional, Norman, Anthony W., additional, Nys, Yves, additional, Onal, Melda, additional, Pal, Lubna, additional, Patterson, Kristine Y., additional, Pauwels, Steven, additional, Pehrsson, Pamela R., additional, Petkovich, Martin, additional, Pettifor, John M., additional, Pfeffer, Paul E., additional, Phillips, Katherine M., additional, Pike, J. Wesley, additional, Pilz, Stefan, additional, Pittas, Anastassios G., additional, Pludowski, Pawel, additional, Prosser, David E., additional, Pullagura, Sri Ramulu N., additional, Quarles, L. Darryl, additional, Rajagopal, Rithwick, additional, Ransohoff, Katherine J., additional, Rauz, Saaeha, additional, Rebolledo, Brian J., additional, Reichrath, Jörg, additional, Rieger, Sandra, additional, Riek, Amy E., additional, Rochel, Natacha, additional, Roizen, Jeffrey D., additional, Roseland, Janet M., additional, Rosen, Cliff, additional, Rybchyn, Mark S., additional, Saitoh, Hiroshi, additional, Salehi-Tabar, Reyhaneh, additional, Schafer, Anne L., additional, Schlingmann, Karl P., additional, Schoenmakers, Inez, additional, Schwartz, Zvi, additional, Scott, Kayla, additional, Sempos, Christopher T., additional, Sepiashvili, Lusia, additional, Seshadri, Mukund, additional, Shane, Elizabeth, additional, Shaurova, Tatiana, additional, Shui, Irene, additional, Silver, Justin, additional, Singh, Ravinder J., additional, Skingle, Linda, additional, St-Arnaud, René, additional, Starr, Jessica, additional, Stayrook, Keith R., additional, Stein, Emily M., additional, Stites, Ryan E., additional, Studzinski, George P., additional, Suda, Tatsuo, additional, Takahashi, Fumiaki, additional, Takahashi, Naoyuki, additional, Tang, Jean Y., additional, Taylor, Christine L., additional, Taylor, Hugh S., additional, Tebben, Peter J., additional, Thacher, Thomas D., additional, Thadhani, Ravi, additional, Thandrayen, Kebashni, additional, Thys-Jacobs, Susan, additional, Tiosano, Dov, additional, Toni, Roberto, additional, Towler, Dwight A., additional, Trump, Donald L., additional, Udagawa, Nobuyuki, additional, Uitterlinden, André G., additional, Unnanuntana, Aasis, additional, van de Peppel, Jeroen, additional, van der Eerden, Bram C.J., additional, van Driel, Marjolein, additional, van Leeuwen, Johannes P.T.M., additional, van Schoor, Natasja, additional, Vanherwegen, An-Sofie, additional, Vazirnia, Aria, additional, Verlinden, Lieve, additional, Verstuyf, Annemieke, additional, Vieth, Reinhold, additional, Wagner, Carol L., additional, Wallace, Graham R., additional, Weaver, Connie, additional, Welsh, JoEllen, additional, White, John H., additional, Whiting, Susan J., additional, Whyte, Michael P., additional, Wysolmerski, John J., additional, Yamada, Sachiko, additional, Yu, Olivia B., additional, Zavala, Kathryn, additional, Zechner, Christoph, additional, Zeytinoglu, Meltem, additional, and Zhao, Hengguang, additional
- Published
- 2018
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3. Contributors
- Author
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Abrams, Steven A., primary, Adams, John S., additional, Adams, Judith E., additional, Adorini, Luciano, additional, Anderson, Paul H., additional, Arab, Lenore, additional, Atkins, Gerald J., additional, Berdal, Ariane, additional, Bhan, Ishir, additional, Bikle, Daniel, additional, Bilezikian, John P., additional, Bischoff-Ferrari, Heike, additional, Boskey, Adele L., additional, Bouillon, Roger, additional, Boyan, Barbara D., additional, Brown, Alex J., additional, Brown, Edward M., additional, Bruce, Danny, additional, Burghardt, Andrew J., additional, Burne, Thomas, additional, Calvo, Mona S., additional, Camargo, Carlos A., additional, Cantorna, Margherita, additional, Carlberg, Carsten, additional, Carpenter, Thomas O., additional, Carson, Matthew W., additional, Ceglia, Lisa, additional, Chen, Hong, additional, Chen, Songcang, additional, Christakos, Sylvia, additional, Coe, Fredric L., additional, Compston, Juliet, additional, Cross, Heide S., additional, Cusano, Natalie E., additional, Dawson-Hughes, Bess, additional, De Clercq, Pierre, additional, DeLuca, Hector, additional, Danilenko, Michael, additional, David, Valentin, additional, Deluca, Hector F., additional, Demay, Marie B., additional, de Paula, Francisco J.A., additional, Descroix, Vianney, additional, Dhawan, Puneet, additional, Dixon, Katie M., additional, Dobnig, Harald, additional, Dodge, Jeffrey A., additional, Donnelly, Eve, additional, Doroudi, Maryam, additional, Dowd, Diane R., additional, Drezner, Marc K., additional, Dusso, Adriana S., additional, Ebeling, Peter R., additional, Edouard, Thomas, additional, Eelen, Guy, additional, Eisman, John A., additional, Epps, Tina, additional, Epstein, Ervin H., additional, Epstein, Sol, additional, Eyles, Darryl, additional, Farach-Carson, Mary C., additional, Favus, Murray J., additional, Feldman, David, additional, Findlay, David M., additional, Fleet, James C., additional, Franceschi, Renny T., additional, Fujiki, Ryoji, additional, Gardner, David G., additional, Ginde, Adit A., additional, Giovannucci, Edward, additional, Glenn, Denis J., additional, Glorieux, Francis H., additional, Gocek, Elzbieta, additional, Goltzman, David, additional, González-Sancho, José Manuel, additional, Gordon-Thomson, Clare, additional, Gysemans, Conny, additional, Hansen, Karen E., additional, Haussler, Carol A., additional, Haussler, Mark R., additional, Hayes, Colleen E., additional, Heaney, Robert P., additional, Helvig, Christian, additional, Hendy, Geoffrey N., additional, Hewison, Martin, additional, Hirsch, Arnold Lippert, additional, Holick, Michael F., additional, Hollis, Bruce W., additional, Holt, Elizabeth, additional, Hsieh, Jui-Cheng, additional, Insogna, Karl L., additional, Johnson, Candace, additional, Jones, Glenville, additional, Jurutka, Peter W., additional, Kalkwarf, Heidi J., additional, Kato, Shigeaki, additional, Kliewer, Steven A., additional, Koeffler, H. Phillip, additional, Korf, Hannelie, additional, Kouzmenko, Alexander, additional, Kovacs, Christopher S., additional, Kream, Barbara E., additional, Kremer, Richard, additional, Krishnan, Aruna V., additional, Krug, Roland, additional, Kubodera, Noboru, additional, Kumar, Rajiv, additional, Laing, Emma M., additional, Lane, Joseph M., additional, Larriba, María Jesús, additional, Lee, Seong Min, additional, Lewis, Richard D., additional, Li, Yan, additional, Li, Yan Chun, additional, Lian, Jane B., additional, Lichtler, Alexander C., additional, Lips, Paul, additional, Liu, Philip T., additional, Lisse, Thomas S., additional, Ma, Yanfei L., additional, MacDonald, Paul N., additional, Mady, Leila, additional, Maggi, Mario, additional, Majumdar, Sharmila, additional, Makishima, Makoto, additional, Malloy, Peter J., additional, Mangelsdorf, David J., additional, Mansbach, Jonathan M., additional, Manson, JoAnn E., additional, Mason, Rebecca S., additional, Mathieu, Chantal, additional, Mayne, Christopher G., additional, McAlindon, Timothy M., additional, McGrath, John, additional, Meyer, Mark B., additional, Mizwicki, Mathew T., additional, Molla, Muriel, additional, Montecino, Martin, additional, Moras, Dino, additional, Morelli, Annamaria, additional, Morris, Howard A., additional, Muñoz, Alberto, additional, Nanes, Mark S., additional, Nashold, Faye E., additional, Naveh-Many, Tally, additional, Ni, Wei, additional, Nelson, Corwin D., additional, Norman, Anthony W., additional, Ohtake, Fumiaki, additional, Okamoto, Ryoko, additional, Okereke, Olivia I., additional, Pal, Lubna, additional, Petkovich, Martin, additional, Pettifor, John M., additional, Pike, J. Wesley, additional, Pittas, Anastassios G., additional, Plum, Lori A., additional, Prosser, David E., additional, Quarles, L. Darryl, additional, Rebolledo, Brian J., additional, Reichrath, Jörg, additional, Rochel, Natacha, additional, Rosen, Clifford J., additional, Ross, F. Patrick, additional, Sambrook, Philip, additional, Schmidt, Daniel R., additional, Schoch, Ryan D., additional, Schwartz, Gary G., additional, Schwartz, Zvi, additional, Sequeira, Vanessa, additional, Shane, Elizabeth, additional, Shea, M. Kyla, additional, Silver, Justin, additional, Simpson, Robert U., additional, Skingle, Linda, additional, Slatopolsky, Eduardo, additional, Sourij, Harald, additional, Spanier, Justin A., additional, Specker, Bonny L., additional, St-Arnaud, René, additional, Stayrook, Keith R., additional, Stein, Emily M., additional, Stein, Gary S., additional, Stein, Janet L., additional, Studzinski, George P., additional, Takahashi, Fumiaki, additional, Tang, Jean Y., additional, Taylor, Hugh S., additional, Tebben, Peter, additional, Thadhani, Ravi, additional, Thiex, Natalie W., additional, Thompson, William R., additional, Thys-Jacobs, Susan, additional, Tiosano, Dov, additional, Towler, Dwight A., additional, Trump, Donald, additional, Uitterlinden, André G., additional, Unnanuntana, Aasis, additional, Vandewalle, Maurits, additional, van Driel, Marjolein, additional, van Leeuwen, Johannes P.T.M., additional, van Wijnen, Andre J., additional, van Schoor, Natasja, additional, Verlinden, Lieve, additional, Verstuyf, Annemieke, additional, Vieth, Reinhold, additional, Weaver, Connie M., additional, Weinstein, Barrie M., additional, Welsh, JoEllen, additional, White, John H., additional, Whitfield, G. Kerr, additional, Whiting, Susan J., additional, Whyte, Michael P., additional, Wysolmerski, John J., additional, Yamada, Sachiko, additional, and Yip, Ian, additional
- Published
- 2011
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4. Analogs of Calcitriol
- Author
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Verlinden, Lieve, primary, Eelen, Guy, additional, Bouillon, Roger, additional, Vandewalle, Maurits, additional, De Clercq, Pierre, additional, and Verstuyf, Annemieke, additional
- Published
- 2011
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5. Contributors
- Author
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Adler, Robert A., primary, Allen, Matthew R., additional, Amin, Shreyasee, additional, Antoniucci, Diana M., additional, Araujo, Andre B., additional, Armas, Laura A.G., additional, Baroncelli, Giampiero I., additional, Bertelloni, Silvano, additional, Bhasin, Shalender, additional, Bilezikian, John P., additional, Binkley, Neil C., additional, Boonen, Steven, additional, Boskey, Adele L., additional, Bouillon, Roger, additional, Burr, David B., additional, Burrows, Melonie, additional, Callewaert, Filip, additional, Carmeliet, Geert, additional, Cianferotti, Luisella, additional, Compston, Juliet, additional, Cosman, Felicia, additional, Cremers, Serge, additional, Davison, K. Shawn, additional, Dempster, David W., additional, Eisman, John A., additional, Fuleihan, Ghada El-Hajj, additional, Eriksen, Erik Fink, additional, Favus, Murray J., additional, Felsenberg, Dieter, additional, Ferrari, Serge, additional, Fyhrie, David P., additional, Garnero, Patrick, additional, Gennari, Luigi, additional, Geusens, Piet, additional, Gilsanz, Vicente, additional, Girotra, Monica, additional, Giusti, Andrea, additional, Giustina, Andrea, additional, Goemaere, Stefan, additional, Gold, Deborah T., additional, Guo, X. Edward, additional, Haentjens, Patrick, additional, Halse, Johan, additional, Handelsman, David J., additional, Haney, Elizabeth M., additional, Hanley, David A., additional, Heaney, Robert P., additional, Jasuja, Ravi, additional, Johansson, Helena, additional, Kanis, John A., additional, Kaufman, Jean-Marc, additional, Klein, Robert, additional, Kousteni, Stavroula, additional, Krueger, Diane, additional, Lakshman, Kishore M., additional, Lang, Thomas F., additional, Lapauw, Bruno, additional, Lappe, Joan M., additional, Leder, Benjamin Z., additional, Lems, Willem, additional, Liu, X. Sherry, additional, Lu, Shi S., additional, Macdonald, Heather M., additional, Maes, Christa, additional, Maloney, Ann E, additional, Cawthon, Peggy Mannen, additional, Marcocci, Claudio, additional, Marshall, Lynn, additional, Mazziotti, Gherardo, additional, McCloskey, Eugene V., additional, McKay, Heather A., additional, Meier, Christian, additional, Miller, Paul D., additional, Misra, Bismruta, additional, Mora, Stefano, additional, Nguyen, Tuan V., additional, Oden, Anders, additional, Ohlsson, Claes, additional, O’Neill, Terence W., additional, Orwoll, Eric S., additional, Papapoulos, Socrates E., additional, Rizzoli, René, additional, Rosen, Clifford J., additional, Runge, Martin, additional, Schousboe, John T., additional, Seeman, Ego, additional, Seibel, Markus J., additional, Sellmeyer, Deborah E., additional, Shane, Elizabeth, additional, Shapiro, Jay R., additional, Silverberg, Shonni J., additional, Silverman, Stuart L., additional, Singh, Rajan, additional, Stein, Emily M., additional, Storer, Thomas W., additional, Szulc, Pawel, additional, Tabbal, Mahmoud, additional, Taes, Youri, additional, Turner, Charles H., additional, Vandenput, Liesbeth, additional, Vanderschueren, Dirk, additional, Venken, Katrien, additional, Verlinden, Lieve, additional, Verstuyf, Annemieke, additional, Wang, Qingju, additional, Weaver, Connie M., additional, Wehrli, Felix W., additional, Wimalawansa, Sunil J., additional, Wiren, Kristine M., additional, Zebaze, Roger, additional, and Zhou, Hua, additional
- Published
- 2010
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6. Vitamin D and Bone
- Author
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Bouillon, Roger, primary, Maes, Christa, additional, Verlinden, Lieve, additional, Carmeliet, Geert, additional, and Verstuyf, Annemieke, additional
- Published
- 2010
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- View/download PDF
7. The Vitamin D Hormone and its Nuclear Receptor: Mechanisms Involved in Bone Biology
- Author
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CARMELIET, GEERT, primary, VERSTUYF, ANNEMIEKE, additional, MAES, CHRISTA, additional, EELEN, GUY, additional, and BOUILLON, ROGER, additional
- Published
- 2006
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8. Contributors
- Author
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Åkesson, Kristina, primary, Alatalo, Sari L., additional, Allison, Susan J., additional, Aly, Ziyad Al, additional, Baldock, Paul A., additional, Bilezikian, John P., additional, Binkley, Neil, additional, Body, Jean-Jacques, additional, Bonjour, Jean-Philippe, additional, Boskey, Adele L., additional, Bouillon, Roger, additional, Brixen, Kim, additional, Bruckner, Peter, additional, Carmeliet, Geert, additional, Clark, Ian M, additional, Croucher, Peter, additional, Delmas, Pierre D., additional, Dempster, David W., additional, Devogelaer, Jean-Pierre, additional, Drezner, Marc K., additional, Eastell, Richard, additional, Eelen, Guy, additional, Eriksen, Erik Fink, additional, Fitzpatrick, Lorraine A., additional, Fuleihan, Ghada El-Hajj, additional, Gardiner, Edith M., additional, Garnero, Patrick, additional, Gay, Renate E., additional, Gay, Steffen, additional, Glorieux, Francis H., additional, Goldring, Mary B., additional, Goldring, Steven R., additional, Goltzman, David, additional, González, Esther A., additional, Grauer, Andreas, additional, Gundberg, Caren M., additional, Hardingham, Tim, additional, Harrison, John R., additional, Heinegård, Dick, additional, Helfrich, M.H., additional, Herzog, Herbert, additional, Horton, M.A., additional, Hulley, Philippa, additional, Jüppner, Harald, additional, Kaija, Helena, additional, Khosla, S., additional, Kraenzlin, Marius E., additional, Kream, Barbara E., additional, Kulak, Carolina A. Moreira, additional, van Leeuwen, Johannes P.T.M., additional, Lensmeyer, Gary L., additional, Lian, Jane B., additional, Lorenzo, Joseph A., additional, Lorenzo, Pilar, additional, Maes, Christa, additional, Manicourt, Daniel-Henri, additional, von der Mark, Klaus, additional, Martin, Kevin J., additional, Martin, T. John, additional, Meier, Christian, additional, van Meurs, Joyce B.J., additional, Millán, José Luis, additional, Monroe, David G., additional, Mulder, Jean E., additional, Murphy, Gillian, additional, Naylor, Kim E., additional, Neidhart, Michel, additional, Nguyen, Tuan V., additional, Nishimoto, Satoru K., additional, Patrikainen, Lila O.T., additional, Pols, Huibert A.P., additional, Raisz, Lawrence G., additional, Ralston, Stuart, additional, Rauch, Frank, additional, Reid, Ian R., additional, Risteli, Juha, additional, Risteli, Leila, additional, Rivadeneira, Fernando, additional, Rizzoli, René, additional, Robins, Simon P., additional, Rosen, Clifford J., additional, Rubin, Mishaela R., additional, Russell, Graham, additional, Saxne, Tore, additional, Schmidt-Gayk, Heinrich, additional, Seeman, Ego, additional, Seibel, Markus J., additional, Shane, Elizabeth, additional, Silverberg, Shonni J., additional, Simkin, Peter A., additional, Sims, Natalie A., additional, Siris, Ethel, additional, Spelsberg, Thomas C., additional, Stein, Gary S., additional, Thonar, Eugene J.-M. A., additional, Uitterlinden, André G., additional, Väänänen, H. Kalervo, additional, Verstuyf, Annemieke, additional, Vihko, Pirkko T., additional, Whyte, Michael P., additional, and Zhou, Hua, additional
- Published
- 2006
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9. Vitamin D Effects on Cell Differentiation and Proliferation
- Author
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Mathieu, Chantal, primary, Verstuyf, Annemieke, additional, Segaert, Siegfried, additional, and Bouillon, Roger, additional
- Published
- 2003
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10. CD-ring modified vitamin D3 analogs and their superagonistic action
- Author
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Eelen, Guy, Muñoz Terol, Alberto, Verstuyf, Annemieke, Eelen, Guy, Muñoz Terol, Alberto, and Verstuyf, Annemieke
- Abstract
Non-steroidal analogs of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] represent a most particular class of analogs because they are either not directly derived from the core 1,25(OH)2D3-structure or they have modifications in the core structure that are so drastic that the steroidal structure is lost. Non-steroidal CD-ring analogs of 1,25(OH)2D3 have been developed to study the role of the central rigid CD-ring system in the biological activity of 1,25(OH)2D3. Here we review the different classes of CD-ring analogs and highlight some representative analogs such as the fluorinated D-ring analogs CD578, WU515 and WY1113 which show markedly increased differentiating activity on human SW480-ADH colon cancer cells, characterized by a stronger induction of the invasion suppressor E-cadherin and a stronger repression of the beta-catenin/TCF target oncogene c-Myc. Correspondingly, CD578, WU515 and WY1113 are more potent inhibitors of beta-catenin/TCF signaling than 1,25(OH)2D3 and induce stronger VDR-coactivator interactions. Underlying the increased biological potency of analog CD578 are additional contacts between the side chain fluorine atoms of the analog with specific residues of helix 12 (H12) of the Vitamin D Receptor (VDR) and subsequent stronger VDR-coactivator interactions.
- Published
- 2010
11. Corrigendum to "Lithocholic acid-based design of noncalcemic vitamin D receptor agonists" [Bioorg. Chem. 111 (2021) 104878].
- Author
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Gaikwad S, González CM, Vilariño D, Lasanta G, Villaverde C, Mouriño A, Verlinden L, Verstuyf A, Peluso-Iltis C, Rochel N, Berkowska K, and Marcinkowska E
- Published
- 2023
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12. Structural analysis and biological activities of C25-amino and C25-nitro vitamin D analogs.
- Author
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Gómez-Bouzó U, Belorusova AY, Rivadulla ML, Santalla H, Verlinden L, Verstuyf A, Ferronato MJ, Curino AC, Facchinetti MM, Fall Y, Gómez G, and Rochel N
- Subjects
- Calcitriol chemistry, Calcitriol pharmacology, Receptors, Calcitriol, Vitamin D pharmacology
- Abstract
Intense synthetic efforts have been directed towards the development of noncalcemic analogs of 1,25-dihydroxyvitamin D
3 . We describe here the structural analysis and biological evaluation of two derivatives of 1,25-dihydroxyvitamin D3 with modifications limited to the replacement of the 25-hydroxyl group by a 25-amino or 25-nitro groups. Both compounds are agonists of the vitamin D receptor. They mediate biological effects similar to 1,25-dihydroxyvitamin D3 , the 25-amino derivative being the most potent one while being less calcemic than 1,25-dihydroxyvitamin D3 . The in vivo properties of the compounds make them of potential therapeutic value., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Inc. All rights reserved.)- Published
- 2023
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13. Lithocholic acid-based design of noncalcemic vitamin D receptor agonists.
- Author
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Gaikwad S, González CM, Vilariño D, Lasanta G, Villaverde C, Mouriño A, Verlinden L, Verstuyf A, Peluso-Iltis C, Rochel N, Berkowska K, and Marcinkowska E
- Subjects
- Dose-Response Relationship, Drug, Humans, Lithocholic Acid chemical synthesis, Lithocholic Acid chemistry, Molecular Structure, Structure-Activity Relationship, Tumor Cells, Cultured, Lithocholic Acid pharmacology, Receptors, Calcitriol agonists
- Abstract
The hypercalcemic effects of the hormone 1α,25-dihydroxyvitamin D
3 (calcitriol) and most of known vitamin D metabolites and analogs call for the development of non secosteroidal vitamin D receptor (VDR) ligands as new selective and noncalcemic agonists for treatment of hyperproliferative diseases. We report on the in silico design and stereoselective synthesis of six lithocholic acid derivatives as well as on the calcemic activity of a potent LCA derivative and its crystallographic structure in complex with zVDR LBD. The low calcemic activity of this compound in comparison with the native hormone makes it of potential therapeutic value. Structure-function relationships provide the basis for the development of even more potent and selective lithocholic acid-based VDR ligands., (Copyright © 2021 Elsevier Inc. All rights reserved.)- Published
- 2021
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14. The proapoptotic protein Bim is up regulated by 1α,25-dihydroxyvitamin D3 and its receptor agonist in endothelial cells and transformed by viral GPCR associated to Kaposi sarcoma.
- Author
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Suares A, Russo de Boland A, Verstuyf A, Boland R, and González-Pardo V
- Subjects
- Alkynes pharmacology, Animals, Bcl-2-Like Protein 11, Caspase 3 metabolism, Cell Line, Transformed, Cholecalciferol pharmacology, Herpesvirus 8, Human genetics, Mice, Receptors, G-Protein-Coupled genetics, Receptors, G-Protein-Coupled metabolism, Viral Proteins genetics, Apoptosis drug effects, Apoptosis Regulatory Proteins biosynthesis, Calcitriol pharmacology, Endothelial Cells metabolism, Herpesvirus 8, Human metabolism, Membrane Proteins biosynthesis, Proto-Oncogene Proteins biosynthesis, Receptors, G-Protein-Coupled agonists, Up-Regulation drug effects, Viral Proteins metabolism
- Abstract
We have previously shown that 1α,25-dihydroxyvitamin D3 [1α,25(OH)2D3] and its less calcemic analog TX 527 induce apoptosis via caspase-3 activation in endothelial cells (SVEC) and endothelial cells transformed by the viral G protein-coupled receptor associated to Kaposi sarcoma (vGPCR). In this work, we studied whether intrinsic apoptotic pathway could be activated by changing the balance between anti and pro-apoptotic proteins. Time response qRT-PCR analysis demonstrated that the mRNA level of anti-apoptotic gene Bcl-2 decreased after 12h and increased after 48h treatment with 1α,25(OH)2D3 or TX 527 in SVEC and vGPCR cells, whereas its protein level remained unchanged through time. mRNA levels of pro-apoptotic gene Bax significantly increased only in SVEC after 24 and 48h treatment with 1α,25(OH)2D3 and TX 527 although its protein levels remained unchanged in both cell lines. Bim mRNA and protein levels increased in SVEC and vGPCR cells. Bim protein increase by 1α,25(OH)2D3 and TX 527 was abolished when the expression of vitamin D receptor (VDR) was suppressed. On the other hand, Bortezomib (0.25-1nM), an inhibitor of NF-κB pathway highly activated in vGPCR cells, increased Bim protein levels and induced caspase-3 cleavage. Altogether, these results indicate that 1α,25(OH)2D3 and TX 527 trigger apoptosis by Bim protein increase which turns into the activation of caspase-3 in SVEC and vGPCR cells. Moreover, this effect is mediated by VDR and involves NF-κB pathway inhibition in vGPCR., (Copyright © 2015 Elsevier Inc. All rights reserved.)
- Published
- 2015
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15. NFκB pathway is down-regulated by 1α,25(OH)(2)-vitamin D(3) in endothelial cells transformed by Kaposi sarcoma-associated herpes virus G protein coupled receptor.
- Author
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Gonzalez-Pardo V, D'Elia N, Verstuyf A, Boland R, and Russo de Boland A
- Subjects
- Boronic Acids pharmacology, Bortezomib, Cell Line, Transformed, Cell Proliferation drug effects, Endothelial Cells metabolism, Endothelial Cells pathology, Gene Expression Regulation, Humans, I-kappa B Proteins genetics, I-kappa B Proteins metabolism, NF-KappaB Inhibitor alpha, NF-kappa B genetics, NF-kappa B metabolism, Protein Transport, Pyrazines pharmacology, Receptors, Calcitriol metabolism, Signal Transduction, Antineoplastic Agents pharmacology, Calcitriol pharmacology, Endothelial Cells drug effects, Herpesvirus 8, Human genetics, I-kappa B Proteins agonists, NF-kappa B antagonists & inhibitors, Receptors, Chemokine genetics, Receptors, Virus genetics
- Abstract
We have previously demonstrated that 1α,25 dihydroxy-vitamin D(3) (1α,25(OH)(2)D(3)) has antiproliferative effects on the growth of endothelial cells transformed by the viral G protein-coupled receptor associated to Kaposi sarcoma (vGPCR). In this work, we have investigated whether 1α,25(OH)(2)D(3) exerts its growth inhibitory effects by inhibiting the Nuclear Factor κ B (NFκB) pathway which is highly activated by vGPCR. Cell proliferation studies demonstrated that 1α,25(OH)(2)D(3), similarly to bortezomib, a proteosome inhibitor that suppresses the activation of NFκB, reduced the proliferation of endothelial cells transformed by vGPCR (SVEC-vGPCR). The activity of NFκB in these cells decreased by 70% upon 1α,25(OH)(2)D(3) treatment. Furthermore, time and dose response studies showed that the hormone significantly decreased NFκB and increased IκBα mRNA and protein levels in SVEC-vGPCR cells, whereas in SVEC only IκBα increased significantly. Moreover, NFκB translocation to the nucleus was inhibited and occurred by a mechanism independent of NFκB association with vitamin D(3) receptor (VDR). 1α,25(OH)(2)D(3)-induced increase in IκBα required de novo protein synthesis, and was independent of MAPK and PI3K/Akt pathways. Altogether, these results suggest that down-regulation of the NFκB pathway is part of the mechanism involved in the antiproliferative effects of 1α,25(OH)(2)D(3) on endothelial cells transformed by vGPCR., (Copyright © 2012 Elsevier Inc. All rights reserved.)
- Published
- 2012
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16. Extraskeletal effects of vitamin D.
- Author
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Wolden-Kirk H, Gysemans C, Verstuyf A, and Mathieu C
- Subjects
- Angiogenesis Inhibitors metabolism, Angiogenesis Inhibitors therapeutic use, Animals, Autoimmune Diseases etiology, Autoimmune Diseases metabolism, Autoimmune Diseases prevention & control, Calcitriol metabolism, Calcitriol therapeutic use, Cardiovascular Diseases etiology, Cardiovascular Diseases genetics, Cardiovascular Diseases metabolism, Cardiovascular Diseases prevention & control, Diabetes Mellitus, Type 1 etiology, Diabetes Mellitus, Type 1 genetics, Diabetes Mellitus, Type 1 metabolism, Diabetes Mellitus, Type 1 prevention & control, Diabetes Mellitus, Type 2 etiology, Diabetes Mellitus, Type 2 metabolism, Diabetes Mellitus, Type 2 prevention & control, Dietary Supplements, Genetic Variation, Humans, Immune System drug effects, Immune System metabolism, Neoplasms drug therapy, Neoplasms etiology, Neoplasms metabolism, Neoplasms prevention & control, Organ Specificity, Receptors, Calcitriol deficiency, Receptors, Calcitriol genetics, Vitamin D therapeutic use, Vitamin D Deficiency metabolism, Vitamin D Deficiency physiopathology, Receptors, Calcitriol metabolism, Signal Transduction, Vitamin D metabolism
- Abstract
The presence of vitamin D receptors in diverse tissues like immune cells, beta-cells in the pancreas, and cardiac myocytes has prompted research to evaluate the impact of vitamin D deficiency on the occurrence of immune diseases, diabetes, and cardiovascular disease (CVD). The expression of receptors not only in normal cells, but also in cancer cells including breast, prostate, and colon cancer cells has moreover opened the path to therapeutic exploitation of vitamin D or its metabolites and hypocalcemic structural analogues as pharmaceutical tools in the fight against chronic non-communicable diseases like diabetes, CVD, and cancer., (Copyright © 2012 Elsevier Inc. All rights reserved.)
- Published
- 2012
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17. Differential sensitivity of epidermal cell subpopulations to beta-catenin-induced ectopic hair follicle formation.
- Author
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Baker CM, Verstuyf A, Jensen KB, and Watt FM
- Subjects
- Animals, Cell Differentiation, Cell Lineage, Epidermal Cells, Epidermis metabolism, Epithelial Cells cytology, Female, Hair Follicle cytology, Male, Mice, Mice, Transgenic, Epithelial Cells metabolism, Hair Follicle growth & development, beta Catenin metabolism
- Abstract
Wnt signalling is required for hair follicle development and for the growth phase (anagen) of postnatal follicles. When the pathway is activated at high levels in adult mouse epidermis, ectopic follicles form from existing follicles, interfollicular epidermis (IFE) and sebaceous glands, revealing a remarkable ability of the tissue to be reprogrammed. To compare the competence of different epidermal cell populations to form ectopic follicles, we expressed a 4-hydroxy-tamoxifen (4OHT) inducible, stabilised beta-catenin transgene (DeltaNbeta-cateninER) under the control of two different promoters. We targeted the reservoir of stem cells in the hair follicle bulge via the keratin 15 (K15) promoter and targeted the sebaceous glands and base of the follicle (bulb) with a truncated K5 promoter (DeltaK5). No ectopic follicles formed in the IFE in either model, establishing the autonomy of the IFE stem cell compartment in undamaged epidermis. Activation of beta-catenin in the bulge stimulated proliferation and bulge expansion. Existing hair follicles entered anagen, but no ectopic follicles formed. DeltaK5DeltaNbeta-cateninER expressing hair follicles also entered anagen on 4OHT treatment. In addition, a subpopulation of cells at the base of the sebaceous gland readily formed ectopic follicles, resulting in complete and reversible conversion of sebaceous glands into hair follicles. Combined activation of beta-catenin and the vitamin D receptor enhanced differentiation of sebaceous gland-derived hair follicles and stimulated ectopic follicle formation in the hair follicle bulb, but not in the bulge. Our results suggest that the bulge and sebaceous gland are, respectively, non-permissive and permissive niches for Wnt induced hair follicle differentiation., (Copyright 2010 Elsevier Inc. All rights reserved.)
- Published
- 2010
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18. Vitamin D: a pleiotropic hormone.
- Author
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Verstuyf A, Carmeliet G, Bouillon R, and Mathieu C
- Subjects
- Animals, Bone and Bones physiology, Calcium physiology, Homeostasis, Humans, Immunologic Factors physiology, Neoplasms etiology, Hormones physiology, Vitamin D physiology, Vitamins physiology, Vitamins therapeutic use
- Abstract
The secosteroid hormone 1alpha,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)) is the natural ligand for the vitamin D receptor, a member of the nuclear receptor superfamily. Upon binding of the ligand, the vitamin D receptor heterodimerizes with the retinoid X receptor and binds to vitamin D response elements in the promoter region of target genes to induce/repress their expression. The target genes that have been identified so far are heterogeneous in nature and reflect the great spectrum of biological activities of 1,25(OH)(2)D(3). Within the last two decades, the receptor has been shown to be present not only in classical target tissues such as bone, kidney, and intestine, but also in many other nonclassical tissues, for example, in the immune system (T and B cells, macrophages, and monocytes), in the reproductive system (uterus, testis, ovary, prostate, placenta, and mammary glands), in the endocrine system (pancreas, pituitary, thyroid, and adrenal cortex), in muscles (skeletal, smooth, and heart muscles), and in brain, skin, and liver. Besides the almost universal presence of vitamin D receptors, different cell types (for example, keratinocytes, monocytes, bone, placenta) are capable of metabolizing 25-hydroxyvitamin D(3) to 1,25(OH)(2)D(3) by the enzyme 25(OH)D(3)-1alpha-hydroxylase, encoded by CYP27B1. The combined presence of CYP27B1 and the specific receptor in several tissues introduced the idea of a paracrine/autocrine role for 1,25(OH)(2)D(3). Moreover, it has been demonstrated that 1,25(OH)(2)D(3) can induce differentiation and inhibit proliferation of normal and malignant cells. Moreover, vitamin D deficiency is associated with an increased risk for nearly all major human diseases such as cancer, autoimmune diseases, cardiovascular, and metabolic diseases. In addition to the treatment of bone disorders with 1,25(OH)(2)D(3), these newly discovered functions open perspectives for the use of 1,25(OH)(2)D(3) as an immune modulator (for example, for the treatment of autoimmune diseases or prevention of graft rejection), inhibitor of cell proliferation, and inducer of cell differentiation (cancer).
- Published
- 2010
- Full Text
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19. Superagonistic fluorinated vitamin D3 analogs stabilize helix 12 of the vitamin D receptor.
- Author
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Eelen G, Valle N, Sato Y, Rochel N, Verlinden L, De Clercq P, Moras D, Bouillon R, Muñoz A, and Verstuyf A
- Subjects
- Binding Sites, Cell Differentiation drug effects, Cell Line, Tumor, Cholecalciferol chemistry, Crystallography, X-Ray, Fluorine Compounds chemistry, Humans, Models, Molecular, Protein Structure, Secondary, Protein Structure, Tertiary, Receptors, Calcitriol genetics, TCF Transcription Factors genetics, Transcription, Genetic drug effects, Transcription, Genetic genetics, beta Catenin genetics, Cholecalciferol agonists, Cholecalciferol analogs & derivatives, Fluorine Compounds agonists, Receptors, Calcitriol chemistry, Receptors, Calcitriol metabolism
- Abstract
Side chain fluorination is often used to make analogs of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] resistant to degradation by 24-hydroxylase. The fluorinated nonsteroidal analogs CD578, WU515, and WY1113 have an increased prodifferentiating action on SW480-ADH colon cancer cells, which correlated with stronger induction of vitamin D receptor (VDR)-coactivator interactions and stronger repression of beta-catenin/TCF activity. Cocrystallization of analog CD578 with the zebrafish (z)VDR and an SRC-1 coactivator peptide showed that the fluorine atoms of CD578 make additional contacts with Val444 and Phe448 of activation helix 12 (H12) of the zVDR and with Leu440 of the H11-H12 loop. Consequently, the SRC-1 peptide makes more contacts with the VDR-CD578 complex than with the VDR-1,25(OH)2D3 complex. These data show that fluorination not only affects degradation of an analog but can also have direct effects on H12 stabilization.
- Published
- 2008
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20. Removal of C-ring from the CD-ring skeleton of 1alpha,25-dihydroxyvitamin D3 does not alter its target tissue metabolism significantly.
- Author
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Reddy GS, Robinson M, Wang G, Palmore GT, Gennaro L, Vouros P, De Clercq P, Vandewalle M, Young W, Ling S, Verstuyf A, and Bouillon R
- Subjects
- Animals, Calcitriol chemical synthesis, Calcitriol pharmacology, Cell Proliferation drug effects, Hypercalcemia drug therapy, Hypercalcemia metabolism, Kidney metabolism, Male, Neoplasms drug therapy, Neoplasms metabolism, Oxidation-Reduction, Rats, Rats, Sprague-Dawley, Vitamins chemical synthesis, Vitamins pharmacology, Calcitriol analogs & derivatives, Calcitriol pharmacokinetics, Vitamins pharmacokinetics
- Abstract
It is now well established that 1alpha,25(OH)2D3 is metabolized in its target tissues through the modifications of both side chain and A-ring. The C-24 oxidation pathway is the side chain modification pathway through which 1alpha,25(OH)2D3 is metabolized into calcitroic acid. The C-3 epimerization pathway is the A-ring modification pathway through which 1alpha,25(OH)2D3 is metabolized into 1alpha,25(OH)2-3-epi-D3. During the past two decades, a great number of vitamin D analogs were synthesized by altering the structure of both side chain and A-ring of 1alpha,25(OH)2D3 with the aim to generate novel vitamin D compounds that inhibit proliferation and induce differentiation of various types of normal and cancer cells without causing significant hypercalcemia. Previously, we used some of these analogs as molecular probes to examine how changes in 1alpha,25(OH)2D3 structure would affect its target tissue metabolism. Recently, several nonsteroidal analogs of 1alpha,25(OH)2D3 with unique biological activity profiles were synthesized. Two of the analogs, SL 117 and WU 515 lack the C-ring of the CD-ring skeleton of 1alpha,25(OH)2D3. SL 117 contains the same side chain as that of 1alpha,25(OH)2D3, while WU 515 contains an altered side chain with a 23-yne modification combined with hexafluorination at C-26 and C-27. Presently, it is unknown how the removal of C-ring from the CD-ring skeleton of 1alpha,25(OH)2D3 would affect its target tissue metabolism. In the present study, we compared the metabolic fate of SL 117 and WU 515 with that of 1alpha,25(OH)2D3 in both the isolated perfused rat kidney, which expresses only the C-24 oxidation pathway and rat osteosarcoma cells (UMR 106), which express both the C-24 oxidation and C-3 epimerization pathways. The results of our present study indicate that SL 117 is metabolized like 1alpha,25(OH)2D3, into polar metabolites via the C-24 oxidation pathway in both rat kidney and UMR 106 cells. As expected, WU 515 with altered side chain structure is not metabolized via the C-24 oxidation pathway. Unlike in rat kidney, both SL 117 and WU 515 are also metabolized into less polar metabolites in UMR 106 cells. These metabolites displayed GC and MS characteristics consistent with A-ring epimerization and were putatively assigned as C-3 epimers of SL 117 and WU 515. In summary, we report that removal of the C-ring from the CD-ring skeleton of 1alpha,25(OH)2D3 does not alter its target tissue metabolism significantly.
- Published
- 2007
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21. Vitamin D resistance.
- Author
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Bouillon R, Verstuyf A, Mathieu C, Van Cromphaut S, Masuyama R, Dehaes P, and Carmeliet G
- Subjects
- Animals, Bile Acids and Salts metabolism, Bone and Bones physiopathology, Calbindins, Calcitriol physiology, Calcium metabolism, Cardiovascular System drug effects, Cell Proliferation drug effects, Child, Humans, Immune System drug effects, Immune System physiology, Intestinal Absorption, Mice, Muscle Weakness etiology, Neoplasms etiology, Phenotype, Rickets physiopathology, S100 Calcium Binding Protein G metabolism, Skin metabolism, Drug Resistance, Receptors, Calcitriol physiology, Vitamin D pharmacology
- Abstract
Vitamin D is a secosteroid of nutritional origin but can also be generated in the skin by ultraviolet light. After two hydroxylations 1,25-(OH)2 vitamin D avidly binds and activates the vitamin D receptor (VDR), a nuclear transcription factor, hereby regulating a large number of genes. The generation of VDR deficient mice has expanded the knowledge on vitamin D from a calcium-regulating hormone to a humoral factor with extensive actions. The effects of the vitamin D system on calcium and bone homeostasis are largely mediated by promoting active intestinal calcium transport via the induction of the epithelial calcium channel TRPV6. Although VDR is redundant in bone, it may regulate the differentiation and function of several bone cells. In skin, VDR expression in keratinocytes is essential in a ligand-independent manner for the maintenance of the normal hair cycle. Therefore, VDR but not vitamin D deficiency results in alopecia. Moreover, 1,25-(OH)2 vitamin D impairs the proliferation not only of keratinocytes but also of many cell types by regulating the expression of cell cycle genes, leading to a G1 cell cycle arrest. In addition, VDR inactivation in mice results in high renin hypertension, cardiac hypertrophy and thrombogenesis. Finally, a dual effect of vitamin D was observed in the immune system where it stimulates the innate immune system while tapering down excessive activation of the acquired immune system. Taken together, the vitamin D endocrine system not only regulates calcium homeostasis but affects several systems mainly by altering gene expression but also by ligand-independent actions.
- Published
- 2006
- Full Text
- View/download PDF
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