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The present study investigates the role of peroxisome proliferator\u2010activated receptor (PPAR) \u03b3 coactivator\u20101\u03b1 (PGC\u20101\u03b1) in cardiac hypertrophy induced by Triiodothyronine (T3). We investigated PGC\u20101\u03b1 mRNA expression in rat hearts exposed to T3 in vivo and ex vivo. Surprisingly, we found that the extended periods of T3 treatment led to an increase in PGC\u20101\u03b1 expression compared to shorter treatment times, which resulted in a reduction of PGC\u20101\u03b1 expression. Mechanistic studies showed that suppression of PGC\u20101\u03b1 by small interfering RNA in cardiomyocytes amplified the cellular hypertrophic response to T3 stimulation, whereas overexpression of PGC\u20101\u03b1 was protective. Furthermore, we presented evidence to show that T3 decreased PGC\u20101\u03b1 expression via p38 mitogen\u2010activated protein kinases (MAPK) pathway. Our studies also revealed that overexpression of PGC\u20101\u03b1 in cardiomyocytes inhibited basal and T3\u2010induced p38 MAPK phosphorylation. These data indicate for the first time that PGC\u20101\u03b1 plays protective role in T3\u2010induced cardiac hypertrophy and that hypertrophic growth induced by T3 involves a regulatory pathway between PGC\u20101\u03b1 and p38 MAPK. J. Cell. Physiol. 227: 3243\u20133253, 2012. \u00a9 2012 Wiley Periodicals, Inc.<\/jats:p>","DOI":"10.1002\/jcp.24015","type":"journal-article","created":{"date-parts":[[2011,11,21]],"date-time":"2011-11-21T13:55:37Z","timestamp":1321883737000},"page":"3243-3253","source":"Crossref","is-referenced-by-count":8,"title":["The protective role of peroxisome proliferator\u2010activated receptor \u03b3 coactivator\u20101\u03b1 in hyperthyroid cardiac 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