{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,17]],"date-time":"2026-08-17T14:45:12Z","timestamp":1786977912596,"version":"build-2736575974"},"reference-count":38,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2010,5,10]],"date-time":"2010-05-10T00:00:00Z","timestamp":1273449600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal Cellular Physiology"],"published-print":{"date-parts":[[2010,11]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Cardiac hypertrophy, which is characterized by an increase in cell size and reactivation of fetal genes, occurs as an adaptive response to diverse forms of stress and often results in heart failure and sudden death. Growing evidence indicates that microRNAs (miRNAs) are involved in cardiac hypertrophy, but the function of these miRNAs remains elusive. Here, using real time PCR analysis, we showed that several miRNAs were dynamically regulated in the rat hypertrophic hearts and miR\u2010199a was up\u2010regulated by 10\u2010fold in hypertrophic hearts after abdominal aorta constriction for 12 weeks. With tissue profiling analysis, we showed that miR\u2010199a was predominantly expressed in cardiomyocytes, but was also faintly detected in cardiac fibroblasts. To investigate whether miR\u2010199a was involved in cardiac hypertrophy, both over\u2010expression and knockdown of miR\u2010199a were performed in cultured cardiomyocytes. Over\u2010expression of miR\u2010199a in cardiomyocytes increased the cell size as measured by cell surface area, and also reduced the mRNA expression level of \u03b1\u2010myosin heavy chain. In accordance, knockdown of endogenous miR\u2010199a in cardiomyocytes reduced the cell size. Down\u2010regulation of miR\u2010199a also attenuated the phenylephrine\u2010induced increase of cell size. Furthermore, bioinformatic algorithms were used to predict the potential targets of miR\u2010199a in cardiac hypertrophy, and hypoxia\u2010inducible factor 1 alpha was confirmed by the luciferase reporter assay to be a potential target of miR\u2010199a. Taken together, our results demonstrated that miR\u2010199a, which was predominantly expressed in cardiomyocytes, was essential for the maintenance of cell size of cardiomyocytes and might play a role in the regulation of cardiac hypertrophy. J. Cell. Physiol. 225: 437\u2013443, 2010. \u00a9 2010 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jcp.22217","type":"journal-article","created":{"date-parts":[[2010,5,10]],"date-time":"2010-05-10T09:05:22Z","timestamp":1273482322000},"page":"437-443","source":"Crossref","is-referenced-by-count":112,"title":["MicroRNAs are dynamically regulated in hypertrophic hearts, and miR\u2010199a is essential for the maintenance of cell size in cardiomyocytes"],"prefix":"10.1002","volume":"225","author":[{"given":"Xiao\u2010Wei","family":"Song","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qing","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Li","family":"Lin","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiao\u2010Chen","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dong\u2010Feng","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guo\u2010Kun","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"An\u2010Jing","family":"Ren","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yan\u2010Rong","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yong\u2010Wen","family":"Qin","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wen\u2010Jun","family":"Yuan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qing","family":"Jing","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2010,5,10]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.01303.2004"},{"key":"e_1_2_6_3_1","doi-asserted-by":"publisher","DOI":"10.1038\/nm1582"},{"key":"e_1_2_6_4_1","doi-asserted-by":"publisher","DOI":"10.1038\/ng1725"},{"key":"e_1_2_6_5_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0710228105"},{"key":"e_1_2_6_6_1","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2007.061170"},{"key":"e_1_2_6_7_1","doi-asserted-by":"publisher","DOI":"10.1093\/eurheartj\/ehp573"},{"key":"e_1_2_6_8_1","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.108.769984"},{"key":"e_1_2_6_9_1","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.108.183087"},{"key":"e_1_2_6_10_1","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.108.182535"},{"key":"e_1_2_6_11_1","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.73.1.184"},{"key":"e_1_2_6_12_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.5.2509"},{"key":"e_1_2_6_13_1","first-page":"191","article-title":"Modulation 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