{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T04:22:08Z","timestamp":1790828528026,"version":"4.1.0"},"reference-count":29,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2018,8,2]],"date-time":"2018-08-02T00:00:00Z","timestamp":1533168000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2018,8,2]],"date-time":"2018-08-02T00:00:00Z","timestamp":1533168000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/100009619","name":"Japan Agency for Medical Research and Development","doi-asserted-by":"publisher","award":["18am0101084j0002"],"award-info":[{"award-number":["18am0101084j0002"]}],"id":[{"id":"10.13039\/100009619","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal Cellular Physiology"],"published-print":{"date-parts":[[2019,2]]},"abstract":"<jats:p>Nuclear factor erythroid 2\u2013related factor 2 (Nrf2) is a master regulator for the induction of antioxidative genes and plays roles in diverse cellular functions. The roles of Nrf2 in muscle regeneration have been investigated, and both important and unimportant roles of Nrf2 for muscle regeneration have been reported. Here, using aged Nrf2\u2010null and Nrf2\u2013dystrophic double\u2010null mice, we showed nonsignificant phenotypes in the muscle regeneration ability of Nrf2\u2010null mice. In contrast with these results, strikingly, almost all Nrf2\u2010null muscle stem cells (MuSCs) isolated by fluorescence\u2010activated cell sorting died in vitro of apoptosis and were not rescued by antioxidative reagents. Although their proliferation was still impaired, the Nrf2\u2010null MuSCs attached to myofibers activated and divided normally, at least in the first round. To elucidate these discrepancies of MuSCs behaviors, we focused on the basal lamina, because both in vivo and single myofiber culture allow MuSCs within the basal lamina to become activated. In a basal lamina\u2013disrupted model, Nrf2\u2010null mice exhibited remarkable regeneration defects without increased levels of reactive oxidative species in MuSCs, suggesting that the existence of the basal lamina affects the survival of Nrf2\u2010null MuSCs. Taken together, these results suggest that the basal lamina compensates for the loss of Nrf2, independent of the antioxidative roles of Nrf2. In addition, experimental conditions might explain the discrepant results of Nrf2\u2010null regenerative ability.<\/jats:p>","DOI":"10.1002\/jcp.27040","type":"journal-article","created":{"date-parts":[[2018,8,6]],"date-time":"2018-08-06T23:31:14Z","timestamp":1533598274000},"page":"1689-1698","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":15,"title":["Implication of basal lamina dependency in survival of Nrf2\u2010null muscle stem cells via an antioxidative\u2010independent mechanism"],"prefix":"10.1002","volume":"234","author":[{"given":"Yusei","family":"Takemoto","sequence":"first","affiliation":[{"name":"Laboratory of Molecular and Cellular Physiology Graduate School of Pharmaceutical Sciences, Osaka University Osaka Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shoya","family":"Inaba","sequence":"additional","affiliation":[{"name":"Laboratory of Molecular and Cellular Physiology Graduate School 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