{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Madhusudhan T"],"funding":["BMBF","Deutscher Akademischer Austauschdienst","DFG","Alexander von Humboldt-Stiftung","National Heart, Lung, and Blood Institute","NHLBI NIH HHS","Boehringer Ingelheim","Stiftung Pathobiochemie und Molekulare Diagnostik"],"pagination":["1762-1780"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7460917"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["31(8)"],"pubmed_abstract":["<h4>Background</h4>Diabetic nephropathy (dNP), now the leading cause of ESKD, lacks efficient therapies. Coagulation protease-dependent signaling modulates dNP, in part <i>via</i> the G protein-coupled, protease-activated receptors (PARs). Specifically, the cytoprotective protease-activated protein C (aPC) protects from dNP, but the mechanisms are not clear.<h4>Methods</h4>A combination of <i>in vitro</i> approaches and mouse models evaluated the role of aPC-integrin interaction and related signaling in dNP.<h4>Results</h4>The zymogen protein C and aPC bind to podocyte integrin-<i>β</i> <sub>3</sub>, a subunit of integrin-<i>α</i> <sub>v</sub> <i>β</i> <sub>3</sub>. Deficiency of this integrin impairs thrombin-mediated generation of aPC on podocytes. The interaction of aPC with integrin-<i"],"journal":["Journal of the American Society of Nephrology : JASN"],"pubmed_title":["Podocyte Integrin-<i>β</i> <sub>3</sub> and Activated Protein C Coordinately Restrict RhoA Signaling and Ameliorate Diabetic Nephropathy."],"pmcid":["PMC7460917"],"funding_grant_id":["IS-67/11-1","C2 SCHA 1082/6-1","KO 5736/1-1","RTG2408/P5","RTG2408/P7","RTG2408/P9","259130777 – SFB 1177","01EO1503","SFB854/B26","236360313 – SFB 1118","MO 1082/7-1","HL 101917","IS-67/8-1","R01 HL101917","01GM1518A","Th1789/1-1","WA 3663/2-1"],"pubmed_authors":["Schaefer L","Ruf W","Dong W","Rana R","Biemann R","Moeller MJ","Gadi I","Mathew A","Wang H","Rezaie AR","Al-Dabet MM","Krishnan S","Zeng-Brouwers J","Ghosh S","Gupta D","Zimmermann S","Reiser J","Madhusudhan T","Elwakiel A","Nazir S","Isermann B","Stoyanov S","Kohli S","Esmon CT"],"additional_accession":[]},"is_claimable":false,"name":"Podocyte Integrin-<i>β</i> <sub>3</sub> and Activated Protein C Coordinately Restrict RhoA Signaling and Ameliorate Diabetic Nephropathy.","description":"<h4>Background</h4>Diabetic nephropathy (dNP), now the leading cause of ESKD, lacks efficient therapies. Coagulation protease-dependent signaling modulates dNP, in part <i>via</i> the G protein-coupled, protease-activated receptors (PARs). Specifically, the cytoprotective protease-activated protein C (aPC) protects from dNP, but the mechanisms are not clear.<h4>Methods</h4>A combination of <i>in vitro</i> approaches and mouse models evaluated the role of aPC-integrin interaction and related signaling in dNP.<h4>Results</h4>The zymogen protein C and aPC bind to podocyte integrin-<i>β</i> <sub>3</sub>, a subunit of integrin-<i>α</i> <sub>v</sub> <i>β</i> <sub>3</sub>. Deficiency of this integrin impairs thrombin-mediated generation of aPC on podocytes. The interaction of aPC with integrin-<i","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020 Aug","modification":"2025-04-04T13:57:20.731Z","creation":"2022-02-11T00:53:24.814Z"},"accession":"S-EPMC7460917","cross_references":{"pubmed":["32709711"],"doi":["10.1681/ASN.2019111163","10.1681/asn.2019111163"]}}