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Your search keyword '"Patel, Kapilkumar"' showing total 9 results
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9 results on '"Patel, Kapilkumar"'

1. Long-term safety and efficacy of tezacaftor–ivacaftor in individuals with cystic fibrosis aged 12 years or older who are homozygous or heterozygous for Phe508del CFTR (EXTEND): an open-label extension study

Author

Gibson, Ronald L., Jr., Rowe, Steven M., Lechtzin, Noah, Ahrens, Richard C., McCoy, Karen S., Aitken, Moira, Donaldson, Scott H., McBennett, Kimberly Ann, Pilewski, Joseph M., Billings, Joanne, Milla, Carlos, Rubenstein, Ronald, Rosenbluth, Daniel Brian, Linnemann, Rachel, Powers, Michael R., Fortner, Christopher, Frederick, Carla Anne, Liou, Theodore G., Black, Philip, Wang, Janice, Colombo, John L., Berdella, Maria, Indihar, Maria Veronica, Brown, Cynthia D., Anstead, Michael, Bilodeau, Lara, Sicilian, Leonard, Jain, Manu, Tolle, James Jerome, Moffett, Kathryn, Nasr, Samya, Taylor-Cousar, Jennifer, Barto, Tara Lynn, Antos, Nicholas, Rogers, John S., Quick, Bryon, Thompson, Henry R., Sawicki, Gregory, Barnett, Bruce, Zanni, Robert L., Smith, Thomas C., Schultz, Karen D., Keating, Claire, Flume, Patrick, Omlor, Gregory J., Ashare, Alix, Voter, Karen, Mehdi, Nighat, Ortiz, Maria Gabriela Tupayachi, Gardner, Tonia E., Boas, Steven R., Messore, Barbara, Zemanick, Edith, Jain, Raksha, McCarthy, Michael, Kissner, Dana G., Patel, Kapilkumar, McNamara, John, Philley, Julie, Berlinski, Ariel, Calimano, Francisco J., Chin, Terry, Conrad, Douglas, Daines, Cori, Raissy, Hengameh H., Keens, Thomas G., Lascano, Jorge E., McWilliams, Bennie, Morrissey, Brian, Reyes, Santiago, Chittivelu, Subramanyam, Hussain, Sabiha, Stone, Arvey, Wallace, James, Klingsberg, Ross, Biller, Julie A., Bui, Stephanie, Sommerburg, Olaf, Bignamini, Elisabetta, Collura, Mirella, Biner, Reta Fischer, Moller, Alexander, Salvatore, Donatello, Belleguic, Chantal, Bentur, Lea, Efrati, Ori, Kerem, Eitan, Prais, Dario, Gallego, Esther Quintana, Barry, Peter, Livnat-Levanon, Galit, Asensi, Jose Ramon Villa, Armstrong, David Stuart, de la Cruz, Oscar Asensio, Gilchrist, Francis, Tullis, Diana Elizabeth, Quon, Bradley, Lands, Larry C., Morrison, Nancy, Lavoie, Annick, Linnane, Barry, Elidemir, Okan, Ringshausen, Felix, Kappler, Matthias, Hebestreit, Helge, Mainz, Jochen, Kiefer, Alexander, Koerner-Rettberg, Cordula, Staab, Doris, Gleiber, Wolfgang, Pressler, Tacjana, Stehling, Florian, Hector, Andreas, Sutharsan, Sivagurunathan, Naehrlich, Lutz, Fischer, Rainald, Downey, Damian, Davies, Jane Carolyn, Ketchell, Robert Ian, Carroll, Mary Patricia, Doe, Simon, MacGregor, Gordon, Nash, Edward Fairbairn, Withers, Nicholas, Peckham, Daniel Gavin, Ledson, Martin James, Kansra, Sonal, Lee, Timothy William Rayner, Delaisi, Bertrand, Rault, Gilles, Le Bihan, Jean, Hubert, Dominique, Fajac, Isabelle, Sermet-Gaudelus, Isabelle, Bakker, Marleen, Arets, Bert, De Boeck, Christiane, Chiron, Raphael, Reix, Philippe, Mainguy, Catherine, van Braeckel, Eva, Malfroot, Anne, Durieu, Isabelle, Dufeu, Nadine Desmazes, Prevotat, Anne, van der Meer, Renske, Merkus, Petrus, Weersink, E.J.M., Gomez-Aguero, Isabel Barrio, Gartner, Silvia, Jover, Amparo Sole, Fernandez, Antonio Alvarez, Cox, Desmond William, McKone, Edward F., Plant, Barry James, Selvadurai, Hiranjan, Bowler, Simon David, Wainwright, Claire Elizabeth, Smith, Daniel, Middleton, Peter Gordon, Wilson, John William, Volpi, Sonia, Colombo, Carla, Fabrizzi, Benedetta, Lucidi, Vincenzina, Cresta, Federico, Cucchiara, Salvatore, Eber, Ernst, Ellemunter, Helmut, Huttegger, Isidor, Hjelte, Lena, Krantz, Christina, Gilljam, Marita, Flume, Patrick A, Downey, Damian G, Brown, Cynthia, De Boeck, Kris, Sawicki, Gregory S, Chang, Philip, Paz-Diaz, Hildegarde, Rubin, Jaime L, Yang, Yoojung, Hu, Xingdi, Pasta, David J, Millar, Stefanie J, Campbell, Daniel, Wang, Xin, Ahluwalia, Neil, Owen, Caroline A, and Wainwright, Claire E

Published
2021
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3. Mast-cell expressed membrane protein-1 is expressed in classical monocytes and alveolar macrophages in idiopathic pulmonary fibrosis and regulates cell chemotaxis, adhesion, and migration in a TGFβ-dependent manner.

Author

Perrot, Carole Y., Karampitsakos, Theodoros, Unterman, Avraham, Adams, Taylor, Marlin, Krystin, Arsenault, Alyssa, Zhao, Amy, Kaminski, Naftali, Katlaps, Gundars, Patel, Kapilkumar, Bandyopadhyay, Debabrata, and Herazo-Maya, Jose D.

Subjects
IDIOPATHIC pulmonary fibrosis, ALVEOLAR macrophages, TRANSFORMING growth factors-beta, MONOCYTES, CELL adhesion, PULMONARY fibrosis, CHEMOKINE receptors
Abstract

Mast-cell expressed membrane protein-1 (MCEMP1) is higher in patients with idiopathic pulmonary fibrosis (IPF) with an increased risk of death. Here we aimed to establish the mechanistic role of MCEMP1 in pulmonary fibrosis. We identified increased MCEMP1 expression in classical monocytes and alveolar macrophages in IPF compared with controls. MCEMP1 is upregulated by transforming growth factor beta (TGFβ) at the mRNA and protein levels in monocytic leukemia THP-1 cells. TGFβ-mediated MCEMP1 upregulation results from the cooperation of SMAD3 and SP1 via concomitant binding to SMAD3/SP1 cis-regulatory elements within the MCEMP1 promoter. We also found that MCEMP1 regulates TGFb-mediated monocyte chemotaxis, adhesion, and migration. Our results suggest that MCEMP1 may regulate the migration and transition of monocytes to monocyte-derived alveolar macrophages during pulmonary fibrosis development and progression. [ABSTRACT FROM AUTHOR]

Published
2024
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8. Mast-Cell Expressed Membrane Protein-1 (MCEMP1) is expressed in classical monocytes and alveolar macrophages in Idiopathic Pulmonary Fibrosis and regulates cell chemotaxis, adhesion, and migration in a TGFβ dependent manner.

Author

Perrot CY, Karampitsakos T, Unterman A, Adams T, Marlin K, Arsenault A, Zhao A, Kaminski N, Katlaps G, Patel K, Bandyopadhyay D, and Herazo-Maya JD

Abstract

Background: Mast-Cell Expressed Membrane Protein-1 (MCEMP1) is higher in Idiopathic Pulmonary Fibrosis (IPF) patients with increased risk of death and poor outcomes. Here we seek to establish the mechanistic role of MCEMP1 in pulmonary fibrosis., Methods: MCEMP1 expression was analyzed by single-cell RNA sequencing, immunofluorescence in Peripheral Blood Mononuclear Cells (PBMC) as well as in lung tissues from IPF patients and controls. Chromatin Immunoprecipitation (ChiP) and Proximity Ligation Assay (PLA) were used to study the transcriptional regulation of MCEMP1 . Transient RNA interference and lentivirus transduction were used to knockdown and knock-in MCEMP1 in THP-1 cells to study chemotaxis, adhesion, and migration. Bulk RNA sequencing was used to identify the mechanisms by which MCEMP1 participates in monocyte function. Active RHO pull-down assay was used to validate bulk RNA sequencing results., Results: We identified increased MCEMP1 expression in classical monocytes and alveolar macrophages in IPF compared to controls. MCEMP1 was upregulated by TGFβ at the mRNA and protein levels in THP-1. TGFβ-mediated MCEMP1 upregulation results from the cooperation of SMAD3 and SP1 via concomitant binding to SMAD3/SP1 cis -regulatory elements within the MCEMP1 promoter. In terms of its function, we found that MCEMP1 regulates TGFβ-mediated monocyte chemotaxis, adhesion, and migration. 400 differentially expressed genes were found to increase after TGFβ stimulation of THP-1, further increased in MCEMP1 knock-in cells treated with TGFβ and decreased in MCEMP1 knockdown cells treated with TGFβ. GO annotation analysis of these genes showed enrichment for positive regulation of RHO GTPase activity and signal transduction. While TGFβ enhanced RHO GTPase activity in THP-1 cells, this effect was attenuated following MCEMP1 knockdown., Conclusion: MCEMP1 is highly expressed in circulating classical monocytes and alveolar macrophages in IPF. MCEMP1 is regulated by TGFβ and participates in the chemotaxis, adhesion, and migration of circulating monocytes by modulating the effect of TGFβ in RHO activity. Our results suggest that MCEMP1 may regulate the migration and transition of monocytes to monocyte-derived alveolar macrophages during pulmonary fibrosis development and progression.

Published
2023
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9. Aberrant Expression of ACO1 in Vasculatures Parallels Progression of Idiopathic Pulmonary Fibrosis.

Author

Fukumoto J, Lin M, Banday MM, Patil SS, Krishnamurthy S, Breitzig M, Soundararajan R, Galam L, Narala VR, Johns C, Patel K, Dunning J, Lockey RF, Sharma NS, and Kolliputi N

Abstract

Rationale: Idiopathic pulmonary fibrosis (IPF) is characterized by mitochondrial dysfunction. However, details about the non-mitochondrial enzymes that sustain the proliferative nature of IPF are unclear. Aconitases are a family of enzymes that sustain metabolism inside and outside mitochondria. It is hypothesized that aconitase 1 (ACO1) plays an important role in the pathogenesis of IPF given that ACO1 represents an important metabolic hub in the cytoplasm. Objectives: To determine if ACO1 expression in IPF lungs shows specific patterns that may be important in the pathogenesis of IPF. To determine the similarities and differences in ACO1 expression in IPF, bleomycin-treated, and aging lungs. Methods: ACO1 expression in IPF lungs were characterized and compared to non-IPF controls by western blotting, immunostaining, and enzymatic activity assay. ACO1-expressing cell types were identified by multicolor immunostaining. Using similar methods, the expression profiles of ACO1 in IPF lungs versus bleomycin-treated and aged mice were investigated. Measurements and main results: Lower lobes of IPF lungs, unlike non-IPF controls, exhibit significantly high levels of ACO1. Most of the signals colocalize with von Willebrand factor (vWF), a lineage marker for vascular endothelial cells. Bleomycin-treated lungs also show high ACO1 expressions. However, most of the signals colocalize with E-cadherin and/or prosurfactant protein C, representative epithelial cell markers, in remodeled areas. Conclusions: A characteristic ACO1 expression profile observed in IPF vasculatures may be a promising diagnostic target. It also may give clues as to how de novo angiogenesis contributes to the irreversible nature of IPF., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Fukumoto, Lin, Banday, Patil, Krishnamurthy, Breitzig, Soundararajan, Galam, Narala, Johns, Patel, Dunning, Lockey, Sharma and Kolliputi.)

Published
2022
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