{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,1]],"date-time":"2026-07-01T18:48:33Z","timestamp":1782931713835,"version":"3.54.5"},"reference-count":30,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2018,12,16]],"date-time":"2018-12-16T00:00:00Z","timestamp":1544918400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Cellular Biochemistry"],"published-print":{"date-parts":[[2019,4]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>MIAT may be implicated in the pathogenesis of age\u2010related hearing loss (AHL). This study aimed to clarify the effect of a MIAT signaling pathway on the risk of AHL.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Terminal deoxynucleotidyl transferase dUTP nick\u2010end labeling assay, auditory brainstem response (ABR) and quantitative hair cell counts were used to compare the hearing functions in different groups of mice. 5,5,6,6\u2010Tetrachloro\u20101,1,3,3\u2010tetraethylbenzimidazolylcarbocyanine iodide (JC\u20101) dye method was used to establish the potential association between mitochondrial dysfunction and aging. Real\u2010time polymerase chain reaction, Western blot analysis, computational analysis, and luciferase assay were conducted to establish a myocardial infarction associated transcript (MIAT) signaling pathway, whose role in the pathogenesis of AHL was further validated by 3\u2010[4,5\u2010dimethylthiazol\u20102\u2010yl]\u20102,5 diphenyl tetrazolium bromide\u00a0(MTT) assay and flow cytometry.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Aged C57BL\/6 mice were associated with a more severe level of hair cell loss, while exhibiting a higher ABR threshold at various frequencies as well as a lower percentage of inner\/outer hair cells. A reduced mitochondrial membrane potential in the cochleae of aged C57BL\/6 mice indicated the presence of mitochondrial dysfunction in these mice. Relative expression of MIAT, Sirtuin1 (SIRT1), and peroxisome proliferator\u2010activated receptor \u03b3 coactivator 1\u03b1 (PGC\u20101\u03b1) was downregulated in aged mice, with microRNA\u201029b (miR\u201029b) being highly expressed. Also, MIAT binds to miR\u201029b, an inhibitor of SIRT1 expression. The regulatory relationship among MIAT, miR\u201029b, and SIRT1 was further validated by comparing the differentiated expression of these factors in cells treated with phosphate\u2010buffered saline\u2009+\u2009H<jats:sub>2<\/jats:sub>O<jats:sub>2,<\/jats:sub> a negative control\u2009+\u2009H<jats:sub>2<\/jats:sub>O<jats:sub>2,<\/jats:sub> MIAT\u2009+\u2009H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>, or H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>\u2009+\u2009anti\u2010miR\u201029b.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>MIAT could elevate the expression of SIRT1\/PGC\u20101\u03b1 via downregulating miR\u201029b. And the downregulated SIRT\/PGC\u20101\u03b1 increased the incidence of AHL via promoting the apoptosis of cochlear hair cells.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jcb.27773","type":"journal-article","created":{"date-parts":[[2018,12,17]],"date-time":"2018-12-17T07:54:53Z","timestamp":1545033293000},"page":"4975-4986","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":23,"title":["Rs1894720 polymorphism in\u00a0MIAT increased susceptibility to age\u2010related hearing loss by modulating the activation of miR\u201029b\/SIRT1\/PGC\u20101\u03b1 signaling"],"prefix":"10.1002","volume":"120","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6911-1986","authenticated-orcid":false,"given":"Shaojuan","family":"Hao","sequence":"first","affiliation":[{"name":"Department of Otorhinolaryngology The First Affiliated Hospital of Zhengzhou University Zhengzhou 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