Tatsuguchi Mariko, Seok Hee Young, Callis Thomas E, Thomson J Michael, Chen Jian-Fu, Newman Martin, Rojas Mauricio, Hammond Scott M, Wang Da-Zhi
Carolina Cardiovascular Biology Center, University of North Carolina, Chapel Hill, NC 27599, USA.
J Mol Cell Cardiol. 2007 Jun;42(6):1137-41. doi: 10.1016/j.yjmcc.2007.04.004. Epub 2007 Apr 14.
MicroRNAs (miRNAs) are a recently discovered class of approximately 22-nucleotide regulatory RNAs that post-transcriptionally regulate gene expression. We have recently demonstrated that muscle-specific miRNAs miR-1 and miR-133 play an important role in modulating muscle proliferation and differentiation. Here, we investigate the involvement of miRNAs in cardiac hypertrophy. We analyzed the global expression of miRNAs in agonist-induced hypertrophic cardiomyocytes as well as in pressure overload-induced hypertrophic hearts and found the miRNA expression profile altered in those hypertrophic conditions. We further show that inhibition of endogenous miR-21 or miR-18b augments hypertrophic growth. Conversely, introduction of functional miR-21 or miR-18b into cardiomyocytes represses myocyte hypertrophy. Together, our studies point to miRNAs as critical regulators of cardiac hypertrophy.
微小RNA（miRNA）是最近发现的一类约22个核苷酸的调控RNA，它们在转录后水平调控基因表达。我们最近证明，肌肉特异性miRNA miR-1和miR-133在调节肌肉增殖和分化中起重要作用。在此，我们研究miRNA在心肌肥大中的作用。我们分析了激动剂诱导的肥大心肌细胞以及压力超负荷诱导的肥大心脏中miRNA的整体表达情况，发现这些肥大状态下miRNA表达谱发生了改变。我们进一步表明，抑制内源性miR-21或miR-18b会增强肥大生长。相反，将功能性miR-21或miR-18b导入心肌细胞可抑制心肌细胞肥大。总之，我们的研究表明miRNA是心肌肥大的关键调节因子。
