{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,30]],"date-time":"2026-10-30T02:01:41Z","timestamp":1793325701334,"version":"4.5.0"},"reference-count":53,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"8","funder":[{"DOI":"10.13039\/100000062","name":"National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["R01-DK083525"],"award-info":[{"award-number":["R01-DK083525"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100006727","name":"University of Kansas Medical Center","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100006727","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000968","name":"American Heart Association","doi-asserted-by":"publisher","award":["19POST34380932"],"award-info":[{"award-number":["19POST34380932"]}],"id":[{"id":"10.13039\/100000968","id-type":"DOI","asserted-by":"publisher"}]},{"name":"University of Kansas Biomedical Research and Training Program","id":[{"id":"https:\/\/ror.org\/001tmjg57","id-type":"ROR","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JASN"],"published-print":{"date-parts":[[2020,8]]},"abstract":"<jats:sec>\n                    <jats:title>Significance Statement<\/jats:title>\n                    <jats:p>\n                      In autosomal dominant polycystic kidney disease (ADPKD), progressive fibrosis contributes to renal failure, leading to ESKD. The vasopressin type-2 receptor (V2R) helps to regulate renal water homeostasis and stimulates cyst expansion in ADPKD. We discovered a novel pathogenic pathway behind V2R regulation of fibrosis in ADPKD kidneys. Epithelial V2R stimulation activates interstitial myofibroblasts, in a paracrine manner, in\n                      <jats:italic toggle=\"yes\">Pkd1<\/jats:italic>\n                      gene knockout (KO) mice. Pharmacologic inhibition and gene knockout studies indicated that V2R regulates myofibroblast activation by a yes-associated protein (YAP)\u2013 and connective tissue growth factor (CCN2)\u2013dependent mechanism. The V2R-YAP-CCN2 molecular axis may present novel pharmacologic targets for control of fibrosis in ADPKD.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Fibrosis is a major cause of loss of renal function in autosomal dominant polycystic kidney disease (ADPKD). In this study, we examined whether vasopressin type-2 receptor (V2R) activity in cystic epithelial cells can stimulate interstitial myofibroblasts and fibrosis in ADPKD kidneys.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We treated\n                      <jats:italic toggle=\"yes\">Pkd1<\/jats:italic>\n                      gene knockout (\n                      <jats:italic toggle=\"yes\">Pkd1<\/jats:italic>\n                      KO) mice with dDAVP, a V2R agonist, for 3 days and evaluated the effect on myofibroblast deposition of extracellular matrix (ECM). We also analyzed the effects of conditioned media from primary cultures of human ADPKD cystic epithelial cells on myofibroblast activation. Because secretion of the profibrotic connective tissue growth factor (CCN2) increased significantly in dDAVP-treated\n                      <jats:italic toggle=\"yes\">Pkd1<\/jats:italic>\n                      KO mouse kidneys, we examined its role in V2R-dependent fibrosis in ADPKD as well as that of yes-associated protein (YAP).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      V2R stimulation using dDAVP increased the renal interstitial myofibroblast population and ECM deposition. Similarly, conditioned media from human ADPKD cystic epithelial cells increased myofibroblast activation\n                      <jats:italic toggle=\"yes\">in vitro<\/jats:italic>\n                      , suggesting a paracrine mechanism. Renal collecting duct\u2013specific gene deletion of\n                      <jats:italic toggle=\"yes\">CCN2<\/jats:italic>\n                      significantly reduced cyst growth and myofibroblasts in\n                      <jats:italic toggle=\"yes\">Pkd1<\/jats:italic>\n                      KO mouse kidneys. We found that YAP regulates\n                      <jats:italic toggle=\"yes\">CCN2<\/jats:italic>\n                      , and YAP inhibition or gene deletion reduces renal fibrosis in\n                      <jats:italic toggle=\"yes\">Pkd1<\/jats:italic>\n                      KO mouse kidneys. Importantly, YAP inactivation blocks the dDAVP-induced increase in myofibroblasts in\n                      <jats:italic toggle=\"yes\">Pkd1<\/jats:italic>\n                      KO kidneys. Further\n                      <jats:italic toggle=\"yes\">in vitro<\/jats:italic>\n                      studies showed that V2R regulates YAP by an ERK1\/2-dependent mechanism in human ADPKD cystic epithelial cells.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Our results demonstrate a novel mechanism by which cystic epithelial cells stimulate myofibroblasts in the pericystic microenvironment, leading to fibrosis in ADPKD. The V2R-YAP-CCN2 cell signaling pathway may present a potential therapeutic target for fibrosis in ADPKD.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1681\/asn.2020020190","type":"journal-article","created":{"date-parts":[[2020,6,17]],"date-time":"2020-06-17T14:47:18Z","timestamp":1592405238000},"page":"1697-1710","source":"Crossref","is-referenced-by-count":40,"title":["Epithelial Vasopressin Type-2 Receptors Regulate Myofibroblasts by a YAP-CCN2\u2013Dependent Mechanism in Polycystic Kidney Disease"],"prefix":"10.1681","volume":"31","author":[{"given":"Nidhi","family":"Dwivedi","sequence":"first","affiliation":[{"name":"The Jared Grantham Kidney Institute, University of Kansas Medical Center, Kansas City, Kansas"},{"name":"Department of Medicine, University of Kansas Medical Center, Kansas City, 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