Institute of Biology and Medicine, Wuhan University of Science and Technology, Wuhan, Hubei, China.
College of Biological Science and Technology,Hubei Minzu University,Enshi, Hubei, China.
J Mol Cell Cardiol. 2020 Feb;139:47-61. doi: 10.1016/j.yjmcc.2019.12.013. Epub 2020 Jan 23.
Cardiac hypertrophy is an early milestone of many heart diseases. LncRNAs often play a leading role in this process. However, its mechanism of action in cardiac hypertrophy has not been fully explained. In a previous study, we showed a new mode by which lncRNA-Mhrt inhibited cardiac hypertrophy by inhibiting myocardin. However, the underlying molecular mechanism remains unclear. This study aims to explore potential action modes of Mhrt in regulating the expression of myocardin in the process of cardiac hypertrophy. Here, we find that Mhrt reduces myocardin expression through KLF4 in vivo and in vitro. Meanwhile, Mhrt promotes the expression of KLF4 through direct binding to miR-145a-5p or inhibiting phosphorylation of KLF4 by forming a complex with KLF4 to prevent the binding of ERK and KLF4, thereby inhibiting myocardin expression and the development of myocardial hypertrophy. Taken together, our findings reveal a new pathway, Mhrt-KLF4-myocardin, that regulates cardiac hypertrophy and revealed additional possible action modes of Mhrt in the occurrence and development of cardiac hypertrophy. The new regulatory pathway serves as a potential therapeutic avenue for cardiac hypertrophy.
心肌肥厚是许多心脏病的早期里程碑。长链非编码 RNA(lncRNA)通常在这个过程中起主导作用。然而,其在心肌肥厚中的作用机制尚未完全阐明。在之前的一项研究中,我们展示了 lncRNA-Mhrt 通过抑制肌球蛋白重链结合蛋白 T(myocardin)抑制心肌肥厚的新模式。然而,其潜在的分子机制仍不清楚。本研究旨在探讨 Mhrt 在调节心肌肥厚过程中心肌球蛋白重链结合蛋白 T 表达的潜在作用模式。在这里,我们发现 Mhrt 通过体内和体外的 Krüppel 样因子 4(KLF4)降低心肌球蛋白重链结合蛋白 T 的表达。同时,Mhrt 通过直接结合 miR-145a-5p 或与 KLF4 形成复合物来抑制 KLF4 的磷酸化,从而阻止 ERK 和 KLF4 的结合,从而抑制心肌球蛋白重链结合蛋白 T 的表达和心肌肥厚的发展。总之,我们的研究结果揭示了一条新的调节通路 Mhrt-KLF4-myocardin,它调节心肌肥厚,并揭示了 Mhrt 在心肌肥厚发生和发展中的额外可能作用模式。这条新的调控通路为心肌肥厚提供了潜在的治疗途径。