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4. Anthrax toxins regulate pain signaling and can deliver molecular cargoes into ANTXR2+ DRG sensory neurons

Author

Yang, Nicole J., Isensee, Jörg, Neel, Dylan V., Quadros, Andreza U., Zhang, Han-Xiong Bear, Lauzadis, Justas, Liu, Sai Man, Shiers, Stephanie, Belu, Andreea, Palan, Shilpa, Marlin, Sandra, Maignel, Jacquie, Kennedy-Curran, Angela, Tong, Victoria S., Moayeri, Mahtab, Röderer, Pascal, Nitzsche, Anja, Lu, Mike, Pentelute, Bradley L., Brüstle, Oliver, Tripathi, Vineeta, Foster, Keith A., Price, Theodore J., Collier, R. John, Leppla, Stephen H., Puopolo, Michelino, Bean, Bruce P., Cunha, Thiago M., Hucho, Tim, and Chiu, Isaac M.

Published
2022
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5. Emergence of nociceptive functionality and opioid signaling in human induced pluripotent stem cell–derived sensory neurons

Author

Röderer, Pascal, primary, Belu, Andreea, additional, Heidrich, Luzia, additional, Siobal, Maike, additional, Isensee, Jörg, additional, Prolingheuer, Jonathan, additional, Janocha, Elke, additional, Valdor, Markus, additional, Hagendorf, Silke, additional, Bahrenberg, Gregor, additional, Opitz, Thoralf, additional, Segschneider, Michaela, additional, Haupt, Simone, additional, Nitzsche, Anja, additional, Brüstle, Oliver, additional, and Hucho, Tim, additional

Published
2023
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6. Anthrax toxins regulate pain signaling and can deliver molecular cargoes into ANTXR2+ DRG sensory neurons

Author

Yang, Nicole J., primary, Isensee, Jörg, additional, Neel, Dylan V., additional, Quadros, Andreza U., additional, Zhang, Han-Xiong Bear, additional, Lauzadis, Justas, additional, Liu, Sai Man, additional, Shiers, Stephanie, additional, Belu, Andreea, additional, Palan, Shilpa, additional, Marlin, Sandra, additional, Maignel, Jacquie, additional, Kennedy-Curran, Angela, additional, Tong, Victoria S., additional, Moayeri, Mahtab, additional, Röderer, Pascal, additional, Nitzsche, Anja, additional, Lu, Mike, additional, Pentelute, Bradley L., additional, Brüstle, Oliver, additional, Tripathi, Vineeta, additional, Foster, Keith A., additional, Price, Theodore J., additional, Collier, R. John, additional, Leppla, Stephen H., additional, Puopolo, Michelino, additional, Bean, Bruce P., additional, Cunha, Thiago M., additional, Hucho, Tim, additional, and Chiu, Isaac M., additional

Published
2021
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8. Endothelial S1P 1 Signaling Counteracts Infarct Expansion in Ischemic Stroke

Author

Nitzsche, Anja, primary, Poittevin, Marine, additional, Benarab, Ammar, additional, Bonnin, Philippe, additional, Faraco, Giuseppe, additional, Uchida, Hiroki, additional, Favre, Julie, additional, Garcia-Bonilla, Lidia, additional, Garcia, Manuela C.L., additional, Léger, Pierre-Louis, additional, Thérond, Patrice, additional, Mathivet, Thomas, additional, Autret, Gwennhael, additional, Baudrie, Véronique, additional, Couty, Ludovic, additional, Kono, Mari, additional, Chevallier, Aline, additional, Niazi, Hira, additional, Tharaux, Pierre-Louis, additional, Chun, Jerold, additional, Schwab, Susan R., additional, Eichmann, Anne, additional, Tavitian, Bertrand, additional, Proia, Richard L., additional, Charriaut-Marlangue, Christiane, additional, Sanchez, Teresa, additional, Kubis, Nathalie, additional, Henrion, Daniel, additional, Iadecola, Costantino, additional, Hla, Timothy, additional, and Camerer, Eric, additional

Published
2021
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9. Paladin is a phosphoinositide phosphatase regulating endosomal VEGFR2 signalling and angiogenesis

Author

Nitzsche, Anja, primary, Pietilä, Riikka, additional, Love, Dominic T, additional, Testini, Chiara, additional, Ninchoji, Takeshi, additional, Smith, Ross O, additional, Ekvärn, Elisabet, additional, Larsson, Jimmy, additional, Roche, Francis P, additional, Egaña, Isabel, additional, Jauhiainen, Suvi, additional, Berger, Philipp, additional, Claesson‐Welsh, Lena, additional, and Hellström, Mats, additional

Published
2020
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10. Anthrax Toxin as a Molecular Platform to Target Nociceptive Neurons and Modulate Pain

Author

Yang, Nicole J., primary, Isensee, Jörg, additional, Neel, Dylan, additional, Liu, Sai Man, additional, Zhang, Han Xiong Bear, additional, Belu, Andreea, additional, Palan, Shilpa, additional, Kennedy-Curran, Angela, additional, Röderer, Pascal, additional, Nitzsche, Anja, additional, Lu, Mike, additional, Pentelute, Bradley L., additional, Brüstle, Oliver, additional, Tripathi, Vineeta, additional, Park, Jin Mo, additional, Collier, R. John, additional, Foster, Keith A., additional, Bean, Bruce P., additional, Leppla, Stephen H., additional, Hucho, Tim, additional, and Chiu, Isaac M., additional

Published
2020
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11. Sphingosine 1-phosphate-regulated transcriptomes in heterogenous arterial and lymphatic endothelium of the aorta

Author

Engelbrecht, Eric, primary, Levesque, Michel V, additional, He, Liqun, additional, Vanlandewijck, Michael, additional, Nitzsche, Anja, additional, Niazi, Hira, additional, Kuo, Andrew, additional, Singh, Sasha A, additional, Aikawa, Masanori, additional, Holton, Kristina, additional, Proia, Richard L, additional, Kono, Mari, additional, Pu, William T, additional, Camerer, Eric, additional, Betsholtz, Christer, additional, and Hla, Timothy, additional

Published
2020
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12. Paladin is a PI(4,5)P2 phosphoinositide phosphatase that regulates endosomal signaling and angiogenesis

Author

Nitzsche, Anja, primary, Pietilä, Riikka, additional, Testini, Chiara, additional, Ninchoji, Takeshi, additional, Smith, Ross O., additional, Ekvärn, Elisabet, additional, Larsson, Jimmy, additional, Roche, Francis P., additional, Egaña, Isabel, additional, Jauhiainen, Suvi, additional, Berger, Philipp, additional, Claesson-Welsh, Lena, additional, and Hellström, Mats, additional

Published
2020
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13. Author response: Sphingosine 1-phosphate-regulated transcriptomes in heterogenous arterial and lymphatic endothelium of the aorta

Author

Engelbrecht, Eric, primary, Levesque, Michel V, additional, He, Liqun, additional, Vanlandewijck, Michael, additional, Nitzsche, Anja, additional, Niazi, Hira, additional, Kuo, Andrew, additional, Singh, Sasha A, additional, Aikawa, Masanori, additional, Holton, Kristina, additional, Proia, Richard L, additional, Kono, Mari, additional, Pu, William T, additional, Camerer, Eric, additional, Betsholtz, Christer, additional, and Hla, Timothy, additional

Published
2019
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14. Sphingosine 1-phosphate-regulated transcriptomes in heterogenous arterial and lymphatic endothelium of the aorta

Author

Engelbrecht, Eric, primary, Levesque, Michel V., additional, He, Liqun, additional, Vanlandewijck, Michael, additional, Nitzsche, Anja, additional, Kuo, Andrew, additional, Singh, Sasha A., additional, Aikawa, Masanori, additional, Holton, Kristina, additional, Proia, Richard L, additional, Kono, Mari, additional, Pu, William T., additional, Camerer, Eric, additional, Betsholtz, Christer, additional, and Hla, Timothy, additional

Published
2019
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15. Anthrax toxins regulate pain signaling and can deliver molecular cargoes into ANTXR2+DRG sensory neurons

Author

Yang, Nicole J., Isensee, Jörg, Neel, Dylan V., Quadros, Andreza U., Zhang, Han-Xiong Bear, Lauzadis, Justas, Liu, Sai Man, Shiers, Stephanie, Belu, Andreea, Palan, Shilpa, Marlin, Sandra, Maignel, Jacquie, Kennedy-Curran, Angela, Tong, Victoria S., Moayeri, Mahtab, Röderer, Pascal, Nitzsche, Anja, Lu, Mike, Pentelute, Bradley L., Brüstle, Oliver, Tripathi, Vineeta, Foster, Keith A., Price, Theodore J., Collier, R. John, Leppla, Stephen H., Puopolo, Michelino, Bean, Bruce P., Cunha, Thiago M., Hucho, Tim, and Chiu, Isaac M.

Abstract

Bacterial products can act on neurons to alter signaling and function. In the present study, we found that dorsal root ganglion (DRG) sensory neurons are enriched for ANTXR2, the high-affinity receptor for anthrax toxins. Anthrax toxins are composed of protective antigen (PA), which binds to ANTXR2, and the protein cargoes edema factor (EF) and lethal factor (LF). Intrathecal administration of edema toxin (ET (PA + EF)) targeted DRG neurons and induced analgesia in mice. ET inhibited mechanical and thermal sensation, and pain caused by formalin, carrageenan or nerve injury. Analgesia depended on ANTXR2 expressed by Nav1.8+or Advillin+neurons. ET modulated protein kinase A signaling in mouse sensory and human induced pluripotent stem cell-derived sensory neurons, and attenuated spinal cord neurotransmission. We further engineered anthrax toxins to introduce exogenous protein cargoes, including botulinum toxin, into DRG neurons to silence pain. Our study highlights interactions between a bacterial toxin and nociceptors, which may lead to the development of new pain therapeutics.

Published
2022
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16. Murine platelet production is suppressed by S1P release in the hematopoietic niche, not facilitated by blood S1P sensing

Author

Niazi, Hira, primary, Zoghdani, Nesrine, additional, Couty, Ludovic, additional, Leuci, Alexandre, additional, Nitzsche, Anja, additional, Allende, Maria L., additional, Mariko, Boubacar, additional, Ishaq, Rameez, additional, Aslan, Yetki, additional, Becker, Pierre Hadrien, additional, Gazit, Salomé L., additional, Poirault-Chassac, Sonia, additional, Decouture, Benoit, additional, Baudrie, Veronique, additional, De Candia, Erica, additional, Kono, Mari, additional, Benarab, Ammar, additional, Gaussem, Pascale, additional, Tharaux, Pierre-Louis, additional, Chun, Jerold, additional, Provot, Sylvain, additional, Debili, Najet, additional, Therond, Patrice, additional, Proia, Richard L., additional, Bachelot-Loza, Christilla, additional, and Camerer, Eric, additional

Published
2019
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17. Paladin is a phosphoinositide phosphatase regulating endosomal VEGFR2 signalling and angiogenesis.

Author

Nitzsche, Anja, Pietilä, Riikka, Love, Dominic T, Testini, Chiara, Ninchoji, Takeshi, Smith, Ross O, Ekvärn, Elisabet, Larsson, Jimmy, Roche, Francis P, Egaña, Isabel, Jauhiainen, Suvi, Berger, Philipp, Claesson‐Welsh, Lena, and Hellström, Mats

Abstract

Cell signalling governs cellular behaviour and is therefore subject to tight spatiotemporal regulation. Signalling output is modulated by specialized cell membranes and vesicles which contain unique combinations of lipids and proteins. The phosphatidylinositol 4,5‐bisphosphate (PI(4,5)P2), an important component of the plasma membrane as well as other subcellular membranes, is involved in multiple processes, including signalling. However, which enzymes control the turnover of non‐plasma membrane PI(4,5)P2, and their impact on cell signalling and function at the organismal level are unknown. Here, we identify Paladin as a vascular PI(4,5)P2 phosphatase regulating VEGFR2 endosomal signalling and angiogenesis. Paladin is localized to endosomal and Golgi compartments and interacts with vascular endothelial growth factor receptor 2 (VEGFR2) in vitro and in vivo. Loss of Paladin results in increased internalization of VEGFR2, over‐activation of extracellular regulated kinase 1/2, and hypersprouting of endothelial cells in the developing retina of mice. These findings suggest that inhibition of Paladin, or other endosomal PI(4,5)P2 phosphatases, could be exploited to modulate VEGFR2 signalling and angiogenesis, when direct and full inhibition of the receptor is undesirable. SYNOPSIS: This study identifies Paladin as a vascular PI(4,5)P2 phosphatase, which restricts VEGFR2 internalization and activation of downstream signaling, thereby dampening angiogenesis. Paladin is a phosphoinositide phosphatase with preference for PI(4,5)P2.VEGF‐A induces co‐localization of Paladin with VEGFR2 in EEA1+ early endosomes.Paladin deficiency promotes increased VEGFR2 phosphorylation, internalization, and ERK1/2 signalling.Increased ERK1/2 signalling in Paladin knockout mice leads to endothelial cell hypersprouting in physiological and pathological retinal angiogenesis. [ABSTRACT FROM AUTHOR]

Published
2021
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18. Verliererinnen der Erneuerung? Die Situation von Frauen im ländlichen Vietnam

Author

Nitzsche, Anja

Abstract

Since the mid-1980s Vietnam has been undergoing a far-reaching transformation process. Up till now it is the economic indicators in particular that point to success of the reforms. Thus it is often overseen that the so called Doi Moi (the "Vietnamese version" of Perestroika) has led to severe social discrepancies. Close examination reveals a widening gap in affluence between urban and rural areas, as well as between women and men. Vietnamese women employed in agriculture still must be regarded as the weakest group within this process of change. Despite their extensive participation in the rural economy, women are partially excluded from the benefits of the reforms. Especially in rural areas women suffer more than men from an increased burden of work, decline in their level of education, the deterioration of the health system as well as their limited access to financial and material resources. The re-orientation of the household economy as basic productive unit causes a revival of traditional attitudes and behaviour, mainly conditioned by Confucianism, which promotes the discrimination against women., Internationales Asienforum, Bd. 29 Nr. 3-4 (1998): Internationales Asienforum

Published
2017
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19. Female mice lacking Pald1 exhibit endothelial cell apoptosis and emphysema

Author

Egaña, Isabel, Kaito, Hiroshi, Nitzsche, Anja, Becker, Lore, Ballester-Lopez, Carolina, Niaudet, Colin, Petkova, Milena, Liu, Wei, Vanlandewijck, Michael, Vernaleken, Alexandra, Klopstock, Thomas, Fuchs, Helmut, Gailus-Durner, Valerie, Hrabe de Angelis, Martin, Rask-Andersen, Helge, Johansson, Henrik J., Lehtiö, Janne, He, Liqun, Yildirim, Ali Ö., and Hellström, Mats

Subjects
Cell- och molekylärbiologi, Cell and Molecular Biology
Abstract

Paladin (Pald1, mKIAA1274 or x99384) was identified in screens for vascular-specific genes and is a putative phosphatase. Paladin has also been proposed to be involved in various biological processes such as insulin signaling, innate immunity and neural crest migration. To determine the role of paladin we have now characterized the Pald1 knock-out mouse in a broad array of behavioral, physiological and biochemical tests. Here, we show that female, but not male, Pald1 heterozygous and homozygous knock-out mice display an emphysema-like histology with increased alveolar air spaces and impaired lung function with an obstructive phenotype. In contrast to many other tissues where Pald1 is restricted to the vascular compartment, Pald1 is expressed in both the epithelial and mesenchymal compartments of the postnatal lung. However, in Pald1 knock-out females, there is a specific increase in apoptosis and proliferation of endothelial cells, but not in non-endothelial cells. This results in a transient reduction of endothelial cells in the maturing lung. Our data suggests that Pald1 is required during lung vascular development and for normal function of the developing and adult lung in a sex-specific manner. To our knowledge, this is the first report of a sex-specific effect on endothelial cell apoptosis. List of authors in thesis manuscript: Egaña I, Nitzsche A, Kaito H, Becker L, Garrett L, Niaudet C, Liu W, Vanlandewijck M, Larsson J, Hrabe de Angelis M, Fuchs H, Gailus-Durner V, Vernaleken A, Klopstock T, Hölter S M, Wurst W, Rask-Andersen H, German Mouse Clinic Consortium, Yildirim A Ö, Hellström M

Published
2017

20. The Role of Paladin in Endothelial Cell Signaling and Angiogenesis

Author

Nitzsche, Anja

Subjects
angiogenesis, endothelium, Cell- och molekylärbiologi, Pald1, vascular permeability, Cell and Molecular Biology, lung, phosphatase
Abstract

Angiogenesis, the formation of new blood vessels from a pre-existing vasculature, is crucial during development and for many diseases including cancer. Despite tremendous progress in the understanding of the angiogenic process, many aspects are still not fully elucidated. Several attempts have been made to identify novel genes involved in endothelial cell biology and angiogenesis. Here we focused on Pald1, a recently identified, vascular-enriched gene encoding paladin. Our in vitro studies indicate that paladin is a lipid phosphatase catalyzing dephosphorylation of phosphatidylinositol phosphates, a process essential for endocytosis and intracellular vesicle trafficking. We confirmed paladin’s vascular expression pattern and revealed a shift from a broad endothelial cell expression during development to an arterial mural cell-restricted expression in several vascular beds in adult mice. Paladin expression in the lung, however, was not restricted to the vasculature, but was also observed in pneumocytes and myofibroblasts. Lungs of female, but not male, Pald1 null mice displayed an obstructive lung phenotype with increased alveolar air sacs that were already apparent early in the alveolarization process. Only endothelial cells, but not other main lung cell types, were affected by loss of paladin. Endothelial cell number was reduced in 4-week old mice, possibly due to increased endothelial turnover in Pald1 deficient lungs. Vascular defects were also found in the retina. Loss of paladin led to reduced retinal vascular outgrowth accompanied by a hyperdense and hypersprouting vascular front. Downstream signaling of the major angiogenic driver, vascular endothelial growth factor receptor 2 (VEGFR2) was sustained in Pald1 null mice, and VEGFR2 degradation was impaired. Furthermore, paladin inhibited endothelial cell junction stability and loss of paladin led to reduced vascular permeability. Whether the differences in VEGFR2 signaling and adherens junction stability are connected remains to be fully explored. The newly identified lipid phosphatase activity of paladin and its specific effects on VEGFR2 signaling and adherens junction stability indicate that paladin may be controlling the endocytic pathway.

Published
2016

21. Pharmacological reversal of a pain phenotype in iPSC-derived sensory neurons and patients with inherited erythromelalgia

Author

Cao, Lishuang, primary, McDonnell, Aoibhinn, additional, Nitzsche, Anja, additional, Alexandrou, Aristos, additional, Saintot, Pierre-Philippe, additional, Loucif, Alexandre J.C., additional, Brown, Adam R., additional, Young, Gareth, additional, Mis, Malgorzata, additional, Randall, Andrew, additional, Waxman, Stephen G., additional, Stanley, Philip, additional, Kirby, Simon, additional, Tarabar, Sanela, additional, Gutteridge, Alex, additional, Butt, Richard, additional, McKernan, Ruth M., additional, Whiting, Paul, additional, Ali, Zahid, additional, Bilsland, James, additional, and Stevens, Edward B., additional

Published
2016
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22. Pharmacological reversal of a pain phenotype in iPSC-derived sensory neurons and patients with inherited erythromelalgia.

Author

Lishuang Cao, McDonnell, Aoibhinn, Nitzsche, Anja, Alexandrou, Aristos, Saintot, Pierre-Philippe, Loucif, Alexandre J. C., Brown, Adam R., Young, Gareth, Mis, Malgorzata, Randall, Andrew, Waxman, Stephen G., Stanley, Philip, Kirby, Simon, Tarabar, Sanela, Gutteridge, Alex, Butt, Richard, McKernan, Ruth M., Whiting, Paul, Ali, Zahid, and Bilsland, James

Subjects
ERYTHROMELALGIA, SODIUM channels, CLINICAL medicine, PLURIPOTENT stem cells, SENSORY neurons
Abstract

The article discusses the treatment of five patients with inherited erythromelalgia (IEM) with a selective compound that blocked the Nav1.7 sodium channel resulting in a decrease in heat-induced pain in most of the patients. A comparison of the severity of the clinical phenotype with the hyperexcitability of the induced pluripotent stem cell (iPSC)-derived sensory neurons is tackled. The sensitivity of the in vitro IEM phenotype to Nav1.7 blockers is also explored.

Published
2016
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23. Paladin (X99384) is expressed in the vasculature and shifts from endothelial to vascular smooth muscle cells during mouse development

Author

Wallgard, Elisabet, primary, Nitzsche, Anja, additional, Larsson, Jimmy, additional, Guo, Xiaoyuan, additional, Dieterich, Lothar C., additional, Dimberg, Anna, additional, Olofsson, Tommie, additional, Pontén, Fredrik C., additional, Mäkinen, Taija, additional, Kalén, Mattias, additional, and Hellström, Mats, additional

Published
2012
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24. Combined RNAi and localization for functionally dissecting long noncoding RNAs

Author

Chakraborty, Debojyoti, primary, Kappei, Dennis, additional, Theis, Mirko, additional, Nitzsche, Anja, additional, Ding, Li, additional, Paszkowski-Rogacz, Maciej, additional, Surendranath, Vineeth, additional, Berger, Nicolas, additional, Schulz, Herbert, additional, Saar, Kathrin, additional, Hubner, Norbert, additional, and Buchholz, Frank, additional

Published
2012
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25. RAD21 Cooperates with Pluripotency Transcription Factors in the Maintenance of Embryonic Stem Cell Identity

Author

Nitzsche, Anja, primary, Paszkowski-Rogacz, Maciej, additional, Matarese, Filomena, additional, Janssen-Megens, Eva M., additional, Hubner, Nina C., additional, Schulz, Herbert, additional, de Vries, Ingrid, additional, Ding, Li, additional, Huebner, Norbert, additional, Mann, Matthias, additional, Stunnenberg, Hendrik G., additional, and Buchholz, Frank, additional

Published
2011
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27. A Genome-Scale RNAi Screen for Oct4 Modulators Defines a Role of the Paf1 Complex for Embryonic Stem Cell Identity

Author

Ding, Li, primary, Paszkowski-Rogacz, Maciej, additional, Nitzsche, Anja, additional, Slabicki, Mikolaj Michal, additional, Heninger, Anne-Kristin, additional, Vries, Ingrid de, additional, Kittler, Ralf, additional, Junqueira, Magno, additional, Shevchenko, Andrej, additional, Schulz, Herbert, additional, Hubner, Norbert, additional, Doss, Michael Xavier, additional, Sachinidis, Agapios, additional, Hescheler, Juergen, additional, Iacone, Roberto, additional, Anastassiadis, Konstantinos, additional, Stewart, A. Francis, additional, Pisabarro, M. Teresa, additional, Caldarelli, Antonio, additional, Poser, Ina, additional, Theis, Mirko, additional, and Buchholz, Frank, additional

Published
2009
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28. Erratum: Corrigendum: BAC TransgeneOmics: a high-throughput method for exploration of protein function in mammals

Author

Poser, Ina, primary, Sarov, Mihail, additional, Hutchins, James R A, additional, Hériché, Jean-Karim, additional, Toyoda, Yusuke, additional, Pozniakovsky, Andrei, additional, Weigl, Daniela, additional, Nitzsche, Anja, additional, Hegemann, Björn, additional, Bird, Alexander W, additional, Pelletier, Laurence, additional, Kittler, Ralf, additional, Hua, Sujun, additional, Naumann, Ronald, additional, Augsburg, Martina, additional, Sykora, Martina M, additional, Hofemeister, Helmut, additional, Zhang, Youming, additional, Nasmyth, Kim, additional, White, Kevin P, additional, Dietzel, Steffen, additional, Mechtler, Karl, additional, Durbin, Richard, additional, Stewart, A Francis, additional, Peters, Jan-Michael, additional, Buchholz, Frank, additional, and Hyman, Anthony A, additional

Published
2008
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29. BAC TransgeneOmics: a high-throughput method for exploration of protein function in mammals

Author

Poser, Ina, primary, Sarov, Mihail, additional, Hutchins, James R A, additional, Hériché, Jean-Karim, additional, Toyoda, Yusuke, additional, Pozniakovsky, Andrei, additional, Weigl, Daniela, additional, Nitzsche, Anja, additional, Hegemann, Björn, additional, Bird, Alexander W, additional, Pelletier, Laurence, additional, Kittler, Ralf, additional, Hua, Sujun, additional, Naumann, Ronald, additional, Augsburg, Martina, additional, Sykora, Martina M, additional, Hofemeister, Helmut, additional, Zhang, Youming, additional, Nasmyth, Kim, additional, White, Kevin P, additional, Dietzel, Steffen, additional, Mechtler, Karl, additional, Durbin, Richard, additional, Stewart, A Francis, additional, Peters, Jan-Michael, additional, Buchholz, Frank, additional, and Hyman, Anthony A, additional

Published
2008
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31. Corrigendum: BAC TransgeneOmics: a high-throughput method for exploration of protein function in mammals.

Author

Poser, Ina, Sarov, Mihail, Hutchins, James R A, Hériché, Jean-Karim, Toyoda, Yusuke, Pozniakovsky, Andrei, Weigl, Daniela, Nitzsche, Anja, Hegemann, Björn, Bird, Alexander W, Pelletier, Laurence, Kittler, Ralf, Hua, Sujun, Naumann, Ronald, Augsburg, Martina, Sykora, Martina M, Hofemeister, Helmut, Zhang, Youming, Nasmyth, Kim, and White, Kevin P

Subjects
GENOMICS
Abstract

A correction to the article "BAC transgeneomics: A high-throughput method for exploration of protein function in mammals," by Ina Poser and colleagues is presented.

Published
2008
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32. Zonation, ligand and dose dependence of S1PR1 signalling in blood and lymphatic vasculature.

Author

Del Gaudio I, Nitzsche A, Boyé K, Bonnin P, Poulet M, Nguyen TQ, Couty L, Ha HTT, Nguyen DT, Cazenave-Gassiot A, Ben Alaya K, Thérond P, Chun J, Wenk MR, Proia RL, Henrion D, Nguyen LN, Eichmann A, and Camerer E

Abstract

Aims: Circulating levels of sphingosine 1-phosphate (S1P), an HDL-associated ligand for endothelial cell (EC) protective S1P receptor-1 (S1PR1), are reduced in disease states associated with endothelial dysfunction. Yet as S1PR1 has high affinity for S1P and can be activated by ligand-independent mechanisms and EC-autonomous S1P production, it is unclear if relative reductions in circulating S1P impact endothelial function. It is also unclear how EC S1PR1 insufficiency, whether induced by ligand deficiency or by S1PR1-directed immunosuppressive therapy, affects different vascular subsets., Methods and Results: We here fine-map the zonation of S1PR1 signalling in the murine blood and lymphatic vasculature, superimpose cell type-specific and relative deficiencies in S1P production to define ligand source- and dose-dependence, and correlate receptor engagement to essential functions. In naïve blood vessels, despite broad expression, EC S1PR1 engagement was restricted to resistance-size arteries, lung capillaries and high-endothelial venules (HEV). Similar zonation was observed for albumin extravasation in EC S1PR1 deficient mice, and brain extravasation was reproduced with arterial EC-selective S1pr1 deletion. In lymphatic EC, S1PR1 engagement was high in collecting vessels and lymph nodes and low in terminal capillaries that drain tissue fluids. While EC S1P production sustained S1PR1 signaling in lymphatics and HEV, hematopoietic cells provided ∼90% of plasma S1P and sustained signaling in resistance arteries and lung capillaries. S1PR1 signaling and endothelial function were both surprisingly sensitive to reductions in plasma S1P with apparent saturation around 50% of normal levels. S1PR1 engagement did not depend on sex or age, but modestly increased in arteries in hypertension and diabetes. Sphingosine kinase (Sphk)-2 deficiency also increased S1PR1 engagement selectively in arteries, which could be attributed to Sphk1-dependent S1P release from perivascular macrophages., Conclusions: This study highlights vessel subtype-specific S1PR1 functions and mechanisms of engagement and supports the relevance of S1P as circulating biomarker for endothelial function., (© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.)

Published
2024
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34. Female mice lacking Pald1 exhibit endothelial cell apoptosis and emphysema.

Author

Egaña I, Kaito H, Nitzsche A, Becker L, Ballester-Lopez C, Niaudet C, Petkova M, Liu W, Vanlandewijck M, Vernaleken A, Klopstock T, Fuchs H, Gailus-Durner V, Hrabe de Angelis M, Rask-Andersen H, Johansson HJ, Lehtiö J, He L, Yildirim AÖ, and Hellström M

Subjects
Animals, Disease Models, Animal, Embryo, Mammalian, Emphysema genetics, Female, Heterozygote, Humans, Lung blood supply, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Phosphoprotein Phosphatases genetics, Sex Factors, Apoptosis physiology, Emphysema pathology, Endothelial Cells pathology, Endothelium, Vascular growth & development, Phosphoprotein Phosphatases metabolism
Abstract

Paladin (Pald1, mKIAA1274 or x99384) was identified in screens for vascular-specific genes and is a putative phosphatase. Paladin has also been proposed to be involved in various biological processes such as insulin signaling, innate immunity and neural crest migration. To determine the role of paladin we have now characterized the Pald1 knock-out mouse in a broad array of behavioral, physiological and biochemical tests. Here, we show that female, but not male, Pald1 heterozygous and homozygous knock-out mice display an emphysema-like histology with increased alveolar air spaces and impaired lung function with an obstructive phenotype. In contrast to many other tissues where Pald1 is restricted to the vascular compartment, Pald1 is expressed in both the epithelial and mesenchymal compartments of the postnatal lung. However, in Pald1 knock-out females, there is a specific increase in apoptosis and proliferation of endothelial cells, but not in non-endothelial cells. This results in a transient reduction of endothelial cells in the maturing lung. Our data suggests that Pald1 is required during lung vascular development and for normal function of the developing and adult lung in a sex-specific manner. To our knowledge, this is the first report of a sex-specific effect on endothelial cell apoptosis.

Published
2017
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