{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T22:03:05Z","timestamp":1789768985977,"version":"4.0.1"},"reference-count":71,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"9","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JASN"],"published-print":{"date-parts":[[2017,9]]},"abstract":"<jats:p>\n                    Nephrotic syndrome is characterized by massive proteinuria and injury of specialized glomerular epithelial cells called podocytes. Studies have shown that, whereas low-concentration thrombin may be cytoprotective, higher thrombin concentrations may contribute to podocyte injury. We and others have demonstrated that\n                    <jats:italic toggle=\"yes\">ex vivo<\/jats:italic>\n                    plasma thrombin generation is enhanced during nephrosis, suggesting that thrombin may contribute to nephrotic progression. Moreover, nonspecific thrombin inhibition has been shown to decrease proteinuria in nephrotic animal models. We thus hypothesized that thrombin contributes to podocyte injury in a protease-activated receptor-specific manner during nephrosis. Here, we show that specific inhibition of thrombin with hirudin reduced proteinuria in two rat nephrosis models, and thrombin colocalized with a podocyte-specific marker in rat glomeruli. Furthermore, flow cytometry immunophenotyping revealed that rat podocytes express the protease-activated receptor family of coagulation receptors\n                    <jats:italic toggle=\"yes\">in vivo<\/jats:italic>\n                    . High-concentration thrombin directly injured conditionally immortalized human and rat podocytes. Using receptor-blocking antibodies and activation peptides, we determined that thrombin-mediated injury depended upon interactions between protease-activated receptor 3 and protease-activated receptor 4 in human podocytes, and between protease-activated receptor 1 and protease-activated receptor 4 in rat podocytes. Proximity ligation and coimmunoprecipitation assays confirmed thrombin-dependent interactions between human protease-activated receptor 3 and protease-activated receptor 4, and between rat protease-activated receptor 1 and protease-activated receptor 4 in cultured podocytes. Collectively, these data implicate thrombinuria as a contributor to podocyte injury during nephrosis, and suggest that thrombin and\/or podocyte-expressed thrombin receptors may be novel therapeutic targets for nephrotic syndrome.\n                  <\/jats:p>","DOI":"10.1681\/asn.2016070789","type":"journal-article","created":{"date-parts":[[2017,4,19]],"date-time":"2017-04-19T20:20:15Z","timestamp":1492633215000},"page":"2618-2630","source":"Crossref","is-referenced-by-count":46,"title":["Thrombin-Induced Podocyte Injury Is Protease-Activated Receptor Dependent"],"prefix":"10.1681","volume":"28","author":[{"given":"Ruchika","family":"Sharma","sequence":"first","affiliation":[{"name":"Center for Clinical and Translational Research, The Research Institute at Nationwide Children\u2019s Hospital,"},{"name":"Division of Hematology, Oncology, and BMT, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Amanda P.","family":"Waller","sequence":"additional","affiliation":[{"name":"Center for Clinical and Translational Research, The Research Institute at Nationwide Children\u2019s Hospital,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shipra","family":"Agrawal","sequence":"additional","affiliation":[{"name":"Center for Clinical and Translational Research, The Research Institute at Nationwide Children\u2019s Hospital,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Katelyn J.","family":"Wolfgang","sequence":"additional","affiliation":[{"name":"Center for Clinical and Translational Research, The Research Institute at Nationwide Children\u2019s Hospital,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hiep","family":"Luu","sequence":"additional","affiliation":[{"name":"Center for Clinical and Translational Research, The Research Institute at Nationwide Children\u2019s Hospital,"},{"name":"Heritage College of Osteopathic Medicine, Ohio University, Athens, Ohio;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Khurrum","family":"Shahzad","sequence":"additional","affiliation":[{"name":"Institute of Clinical Chemistry and Pathobiochemistry, Otto-von-Guericke University, Magdeburg, Germany;"},{"name":"Department of Biotechnology, University of Sargodha, Sargodha, Pakistan; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Berend","family":"Isermann","sequence":"additional","affiliation":[{"name":"Institute of Clinical Chemistry and Pathobiochemistry, Otto-von-Guericke University, Magdeburg, Germany;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"William E.","family":"Smoyer","sequence":"additional","affiliation":[{"name":"Center for Clinical and Translational Research, The Research Institute at Nationwide Children\u2019s Hospital,"},{"name":"Division of Nephrology, Nationwide Children\u2019s Hospital, Columbus, Ohio;"},{"name":"Department of Pediatrics, College of Medicine, The Ohio State University, Columbus, Ohio;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marvin T.","family":"Nieman","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Case Western Reserve University, Cleveland, Ohio"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bryce A.","family":"Kerlin","sequence":"additional","affiliation":[{"name":"Center for Clinical and Translational Research, The Research Institute at Nationwide Children\u2019s Hospital,"},{"name":"Division of Hematology, Oncology, and BMT, and"},{"name":"Department of Pediatrics, College of Medicine, The Ohio State University, Columbus, Ohio;"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","published-online":{"date-parts":[[2017,4,19]]},"reference":[{"key":"B1-20230819","first-page":"1","article-title":"Deaths: Final data for 2010. 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