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However, for reasons yet unknown, adaptation to hypoxia through hypoxia\u2010inducible factor (<jats:styled-content style=\"fixed-case\">HIF<\/jats:styled-content>) is limited. Here, we studied miR\u201022, a potential <jats:styled-content style=\"fixed-case\">HIF<\/jats:styled-content> repressor, in normal kidneys, as well as in rhabdomyolysis\u2010induced <jats:styled-content style=\"fixed-case\">AKI<\/jats:styled-content>, a condition where miR\u201022 is up\u2010regulated.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p><jats:styled-content style=\"fixed-case\">AKI<\/jats:styled-content> in mice was provoked by <jats:styled-content style=\"fixed-case\">IM<\/jats:styled-content> injection of glycerol. Tissue homogenates were processed to determine the levels of candidate <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>s and proteins, as well as global gene expression profiles. Reporter assays quantified in vitro miR\u201022 activity and its modulation by mimic or inhibitor molecules, under normoxia or hypoxia (1% O<jats:sub>2<\/jats:sub>) respectively. In vivo, anti\u2013miR\u201022 molecules were applied to normal mice or prior to induction of <jats:styled-content style=\"fixed-case\">AKI<\/jats:styled-content>. Renal outcome was assessed by measuring plasma creatinine, plasma urea and the levels of the injury markers Kim\u20101 and Ngal.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Renal miR\u201022 is inducible by hypoxia and represses hypoxia\u2010inducible factor (<jats:styled-content style=\"fixed-case\">HIF<\/jats:styled-content>). Specific inhibition of miR\u201022 regulates 1913 gene transcripts in kidneys controls and 3386 in AKI, many of which are involved in development or carcinogenesis. Specific inhibition of miR\u201022 up\u2010regulates tissue protective <jats:styled-content style=\"fixed-case\">HIF<\/jats:styled-content> target genes, yet renal function and injury markers are unchanged or worsened.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>miR\u201022 is a <jats:styled-content style=\"fixed-case\">HIF<\/jats:styled-content> repressor constitutively expressed in the adult kidney and up\u2010regulated in <jats:styled-content style=\"fixed-case\">AKI<\/jats:styled-content>. Specific inhibition of miR\u201022 is efficient in vivo and profoundly affects renal gene expression in health and disease, including up\u2010regulation of <jats:styled-content style=\"fixed-case\">HIF<\/jats:styled-content>. However, the net effect on rhabdomyolysis\u2010induced <jats:styled-content style=\"fixed-case\">AKI<\/jats:styled-content> outcome is neutral or even negative.<\/jats:p><\/jats:sec>","DOI":"10.1111\/apha.13102","type":"journal-article","created":{"date-parts":[[2018,5,23]],"date-time":"2018-05-23T16:59:05Z","timestamp":1527094745000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["A dual role of miR\u201022 in rhabdomyolysis\u2010induced acute kidney injury"],"prefix":"10.1111","volume":"224","author":[{"given":"S.","family":"Mathia","sequence":"first","affiliation":[{"name":"Department of Vegetative Physiology Charit\u00e9 \u2013 Universit\u00e4tsmedizin Berlin Corporate Member of Freie Universit\u00e4t Berlin Humboldt\u2010Universit\u00e4t zu Berlin, and Berlin Institute of Health Berlin Germany"},{"name":"Department of Nephrology and Medical Intensive Care Charit\u00e9 \u2013 Universit\u00e4tsmedizin Berlin Corporate Member of Freie Universit\u00e4t Berlin Humboldt\u2010Universit\u00e4t zu Berlin, and Berlin Institute of Health Berlin Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"L. J.","family":"Rudigier","sequence":"additional","affiliation":[{"name":"Department of Biology Humboldt\u2010Universit\u00e4t zu Berlin Berlin Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M.","family":"Kasim","sequence":"additional","affiliation":[{"name":"Department of Vegetative Physiology Charit\u00e9 \u2013 Universit\u00e4tsmedizin Berlin Corporate Member of Freie Universit\u00e4t Berlin Humboldt\u2010Universit\u00e4t zu Berlin, and Berlin Institute of Health Berlin Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0226-8636","authenticated-orcid":false,"given":"K. 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