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Gain of TRPC6 function and loss of podocin function induce podocyte injury. We have previously shown that high glucose induces apoptosis of podocytes by activating TRPC6; however, whether the activated TRPC6 can alter podocin expression remains unknown. Western blot analysis and confocal microscopy were used to examine both expression levels of TRPC6, podocin, and nephrin and morphological changes of podocytes in response to high glucose. High glucose increased the expression of TRPC6 but reduced the expression of podocin and nephrin, in both cultured human podocytes and type 1 diabetic rat kidneys. The decreased podocin was diminished in TRPC6 knockdown podocytes. High glucose elevated intracellular Ca<jats:sup>2+<\/jats:sup>in control podocytes but not in TRPC6 knockdown podocytes. High glucose also elevated the expression of a tight junction protein, zonula occludens-1, and induced the redistribution of zonula occludens-1 and loss of podocyte processes. These data together suggest that high glucose reduces protein levels of podocin by activating TRPC6 and induces morphological changes of cultured podocytes.<\/jats:p>","DOI":"10.1152\/ajprenal.00215.2019","type":"journal-article","created":{"date-parts":[[2019,9,30]],"date-time":"2019-09-30T14:24:06Z","timestamp":1569853446000},"page":"F1605-F1611","source":"Crossref","is-referenced-by-count":22,"title":["High glucose reduces expression of podocin in cultured human podocytes by stimulating TRPC6"],"prefix":"10.1152","volume":"317","author":[{"given":"Xiao-Yu","family":"Lu","sequence":"first","affiliation":[{"name":"Department of Neurology, the Second Affiliated Hospital of Harbin Medical University, Harbin, People\u2019s Republic of China"},{"name":"Department of Physiology, Emory University School of Medicine, Atlanta, Georgia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bing-Chen","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of 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