Research Paper Volume 11, Issue 20 pp 8792—8809
Long non-coding RNA MALAT1 promotes cardiac remodeling in hypertensive rats by inhibiting the transcription of MyoD
- 1 Department of Cardiology, The Affiliated Hospital of Qingdao University, Qingdao 266100, P. R. China
- 2 Department of Endocrinology, The People’s Hospital of Pingdu, Qingdao 266700, P. R. China
- 3 Department of General Medicine, The People's Hospital of Shinan, Qingdao 266002, P. R. China
- 4 Department of Endocrinology, The Affiliated Hospital of Qingdao University, Qingdao 266003, P. R. China
- 5 Department of Urology Surgery, The Affiliated Hospital of Qingdao University, Qingdao 266003, P. R. China
- 6 Department of Geriatrics, The Affiliated Hospital of Qingdao University, Qingdao 266003, P. R. China
received: April 19, 2019 ; accepted: September 2, 2019 ; published: October 15, 2019 ;https://doi.org/10.18632/aging.102265
How to Cite
Copyright © 2019 Li et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Hypertension is the leading preventable cause of premature deaths worldwide. Although long non-coding RNA (lncRNA) metastasis associated lung adenocarcinoma transcript 1 (MALAT1) has been identified to play important roles in the development of cardiovascular diseases, the regulatory function of lncRNA MALAT1 in hypertension remains poorly understood. This study aimed to explore the role of lncRNA MALAT1 in spontaneously hypertensive rats (SHRs). LncRNA MALAT1 was determined to be elevated and MyoD to be reduced in myocardial tissues and thoracic aortic vascular tissues of SHRs. Over-expression of lncRNA MALAT1 caused severe myocardial fibrosis in SHRs. In addition, lncRNA MALAT1 over-expression in vitro enhanced arterial smooth muscle cells (ASMCs) activity and fibrosis of SHRs, which, was rescued by over-expressed MyoD. Furthermore, lncRNA MALAT1 transcripts were found to be highly enriched in the nucleus, and lncRNA MALAT1 suppressed the transactivation of MyoD. Moreover, lncRNA MALAT1 was found to recruit Suv39h1 to MyoD-binding loci, leading to H3K9me3 trimethylation and down-regulation of the target gene. Taken conjointly, this study revealed an important role of lncRNA MALAT1 in promoting cardiac remodeling in hypertensive rats by inhibiting the transcription of MyoD. These results highlight the value of lncRNA MALAT1 as a therapeutic target for the management of hypertension.