{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T04:15:57Z","timestamp":1791000957828,"version":"4.1.0"},"reference-count":30,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2019,4,25]],"date-time":"2019-04-25T00:00:00Z","timestamp":1556150400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2019,4,25]],"date-time":"2019-04-25T00:00:00Z","timestamp":1556150400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal Cellular Physiology"],"published-print":{"date-parts":[[2019,11]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Podocyte damage is a hallmark of diabetic nephropathy (DN). Accumulating evidence indicates that microRNAs play important roles in the DN pathogenesis. This study aimed to explore the possible roles and underlying mechanisms of miR\u201015b\u20105p on high glucose (HG)\u2010triggered podocyte injury. We observed that miR\u201015b\u20105p declined dramatically in a time\u2010dependent manner in podocytes exposed to HG. In addition, miR\u201015b\u20105p restored cell proliferation in HG\u2010induced podocytes. Meanwhile, forced expression of miR\u201015b\u20105p apparently restrained HG\u2010triggered apoptosis of podocytes, concomitant with downregulated in the proapoptotic protein markers Bax and cleavage caspase\u20103, and upregulated the antiapoptotic protein Bcl\u20102. Simultaneously, introduction of miR\u201015b\u20105p repressed HG\u2010induced oxidative stress damage in HG\u2010treated podocytes, as evidenced by reduced MDA content, NOX4 expression, and enhanced activities of superoxide dismutase and catalase. Moreover, enforced expression of miR\u201015b\u20105p remarkably restrained the HG\u2010stimulated inflammatory response, as reflected by attenuated the level of the cytokines IL\u20101\u03b2, TNF\u2010\u03b1, and IL\u20106. More important, we also identified Sema3A as a direct target of miR\u201015b\u20105p. Reverse transcription polymerase chain reaction and western blot subsequently confirmed that miR\u201015b\u20105p negatively modulated the level of Sema3A. Mechanically, overexpression of Sema3A impeded the beneficial effects of miR\u201015b\u20105p on HG\u2010mediated apoptosis, oxidative stress, and inflammatory response. Altogether, these findings manifested that miR\u201015b\u20105p protectively antagonized HG\u2010triggered podocyte damage through relieving HG\u2010induced apoptosis, oxidative stress, and inflammatory process in podocytes by targeting Sema3A, suggesting that miR\u201015b\u20105p might be a new therapeutic agent to improve management of DN.<\/jats:p>","DOI":"10.1002\/jcp.28691","type":"journal-article","created":{"date-parts":[[2019,4,26]],"date-time":"2019-04-26T01:54:33Z","timestamp":1556243673000},"page":"20869-20878","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":60,"title":["miR\u201015b\u20105p ameliorated high glucose\u2010induced podocyte injury through repressing apoptosis, oxidative stress, and inflammatory responses by targeting Sema3A"],"prefix":"10.1002","volume":"234","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5605-9392","authenticated-orcid":false,"given":"Yanqin","family":"Fu","sequence":"first","affiliation":[{"name":"Department of Endocrinology the Second Affiliated Hospital of Zhengzhou University Zhengzhou Henan PR China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chongxian","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Endocrinology the Second Affiliated Hospital of Zhengzhou University Zhengzhou Henan PR China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dongming","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Endocrinology the Second Affiliated Hospital of Zhengzhou University Zhengzhou Henan PR China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaojing","family":"Chu","sequence":"additional","affiliation":[{"name":"Department of Endocrinology the Second Affiliated 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