{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,13]],"date-time":"2026-01-13T00:41:29Z","timestamp":1768264889101,"version":"3.49.0"},"reference-count":33,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2018,11,28]],"date-time":"2018-11-28T00:00:00Z","timestamp":1543363200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"Scientific Research Project of Shanghai Municipal Commission of Health and Family Planning","award":["20164Y0234"],"award-info":[{"award-number":["20164Y0234"]}]},{"name":"Research Fund of Intersection of Medical and Biomedical Engineering, Shanghai Jiaotong University","award":["YG2016QN27"],"award-info":[{"award-number":["YG2016QN27"]}]},{"name":"Special funds for clinical medical research of Chinese Medical Association-Servier nephropathy research program","award":["17010080677"],"award-info":[{"award-number":["17010080677"]}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Cellular Biochemistry"],"published-print":{"date-parts":[[2019,3]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Dysfunction of the peritoneum as a dialysis organ may result from progressive membrane injury on peritoneal dialysis (PD). It has been increasingly recognized that the human peritoneal mesothelial cells (HPMCs) play a key role in peritoneal membrane early injury. Recently, it has been reported that bioincompatible PD fluid with high concentrations of glucose and glucose degradation products, low pH, high osmolality, and peritonitis stimulates HPMCs to release endothelin\u20101 (ET\u20101). ET\u20101 causes increased the release of vascular endothelial growth factor, which is important for tumor cell angiogenesis. We hypothesized that activating ET\u20101 might predict injury of peritoneal membrane.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>HPMCs were isolated from normal omentum. ERK1\/2 and Ets\u20101 phosphorylation were measured by Western blot analysis. HPMC proliferation was detected by the bromodeoxyuridine (BrdU) assay. Capillary networks of tubes formed were photographed under a microscope, and five randomly selected fields from each well were analyzed for total capillary length by using Image J software.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>MEK\u20101 blocker significantly abolished the ERK1\/2 activation by ET\u20101, which also triggered phosphorylation, thus activating the transcription factor Ets\u20101 downstream from ERK1\/2. ET\u20101 was capable to induce HPMC proliferation, which could be attenuated by ET\u20101 antagonists. Antibody and small interfering RNA mediated blockade of Ets\u20101 had similar antiproliferative effects. Thus, ET\u20101 specifically triggered HPMC proliferation via ERK1\/2\u2010Ets\u20101 signaling pathway. VEGF production and endothelial cell angiogenesis were significantly in response to conditioned medium from HPMCs treated with ET\u20101.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>ET\u20101 triggered HPMC proliferation through the ERK1\/2\u2010Ets\u20101 signaling pathway and contributed to VEGF production and endothelial cell angiogenesis.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jcb.27631","type":"journal-article","created":{"date-parts":[[2018,11,28]],"date-time":"2018-11-28T19:11:24Z","timestamp":1543432284000},"page":"3539-3546","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["Endothelin\u20101 triggers human peritoneal mesothelial cells\u2019 proliferation via ERK1\/2\u2010Ets\u20101 signaling pathway and contributes to endothelial cell angiogenesis"],"prefix":"10.1002","volume":"120","author":[{"given":"Nan","family":"Zhu","sequence":"first","affiliation":[{"name":"Department 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