Back to Search
Start Over
MicroRNA-214 modulates the senescence of vascular smooth muscle cells in carotid artery stenosis.
- Source :
-
Molecular Medicine . 5/14/2020, Vol. 26 Issue 1, p1-12. 12p. - Publication Year :
- 2020
-
Abstract
- Background: MicroRNAs control gene expression by post-transcriptional inhibition. Dysregulation of the expressions of miR-199a/214 cluster has been linked to cardiovascular diseases. This study aimed at identifying potential microRNAs related to vascular senescence. Methods: Seven candidate microRNAs (miR-19a, −20a, −26b, −106b, − 126, − 214, and − 374) related to cell proliferation were tested for their expressions under CoCl2-induced hypoxia in vascular smooth muscle cells (VSMCs). After identification of miR-214 as the candidate microRNA, telomere integrity impairment and cell cycle arrest were examined in VSMCs by using miR-214 mimic, AntagomiR, and negative controls. To investigate the clinical significance of miR-214 in vascular diseases, its plasma level from patients with carotid artery stenosis (CAS) was assessed by quantitative reverse transcriptase polymerase chain reaction (qRT-PCR). Results: CoCl2 treatment for 48 h suppressed cell proliferation and angiogenesis as well as enhanced cell senescence in VSMCs. Besides, miR-214 level was elevated in both intracellular and exosome samples of VSMCs after CoCl2 treatment. Manipulating miR-214 in VSMCs demonstrated that miR-214 not only inhibited angiogenic and proliferative capacities but also promoted senescence through the suppression of quaking. Additionally, circulating miR-214 level was upregulated in CAS patients with high low-density lipoprotein cholesterol (LDL-C) value. Conclusion: Our findings suggested that miR-214 plays a role in the modulation of VSMC angiogenesis, proliferation, and senescence with its plasma level being increased in CAS patients with elevated LDL-C value, implying that it may be a vascular senescence marker and a potential therapeutic target for vascular diseases. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 10761551
- Volume :
- 26
- Issue :
- 1
- Database :
- Academic Search Index
- Journal :
- Molecular Medicine
- Publication Type :
- Academic Journal
- Accession number :
- 143225538
- Full Text :
- https://doi.org/10.1186/s10020-020-00167-1