Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2020 Aug;76(2):151-158.
doi: 10.1097/FJC.0000000000000853.

LOXL1-AS1/miR-515-5p/STAT3 Positive Feedback Loop Facilitates Cell Proliferation and Migration in Atherosclerosis

Affiliations

LOXL1-AS1/miR-515-5p/STAT3 Positive Feedback Loop Facilitates Cell Proliferation and Migration in Atherosclerosis

Qiong Xie et al. J Cardiovasc Pharmacol. 2020 Aug.

Abstract

Existing research has elucidated the critical role of long noncoding RNAs (lncRNAs) in the progression of multiple human cardiovascular diseases, including atherosclerosis (AS). Nonetheless, whether long noncoding RNA LOXL1 antisense RNA 1 (LOXL1-AS1) regulates the biological functions in AS is exceedingly limited. In this research, we detected through reverse transcription-quantitative polymerase chain reaction that LOXL1-AS1 expression was markedly upregulated in patients with AS. The role of LOXL1-AS1 in vascular smooth muscle cells (VSMCs) and human umbilical vein endothelial cells (HUVECs) was unmasked by functional assays. Moreover, knockdown of LOXL1-AS1 exerted suppressive effect on proliferation and migration whereas accelerated apoptosis in VSMCs and HUVECs. Molecular mechanism assays revealed that signal transducer and activator of transcription 3 (STAT3) functioned as a transcription activator of LOXL1-AS1 in VSMCs and HUVECs. In addition, miR-515-5p was manifested to bind with LOXL1-AS1 (or STAT3) in VSMCs and HUVECs. Furthermore, LOXL1-AS1 could elevate STAT3 expression by sponging miR-515-5p in VSMCs and HUVECs. More importantly, rescue assays delineated that inhibited expression of miR-515-5p or elevated expression of STAT3 could reverse the restraining effect of LOXL1-AS1 depletion on the progression of AS in HUVECs. All these findings revealed the role of a LOXL1-AS1/miR-515-5p/STAT3 positive feedback loop in AS.

PubMed Disclaimer

Comment in

References

    1. Mozaffarian D, Benjamin EJ, Go AS, et al. Heart disease and stroke statistics-2016 update: a report from the American Heart Association. Circulation. 2016;133:e38–360.
    1. Cui Y, Qi X, Huang A, et al. Differential and predictive value of galectin-3 and soluble suppression of tumorigenicity-2 (sST2) in heart failure with preserved ejection fraction. Med Sci Monit. 2018;24:5139–5146.
    1. Li J, Cui Y, Huang A, et al. Additional diagnostic value of growth differentiation factor-15 (GDF-15) to N-terminal B-type natriuretic peptide (NT-proBNP) in patients with different stages of heart failure. Med Sci Monit. 2018;24:4992–4999.
    1. Jang JH, Kim EA, Park HJ, et al. Methylglyoxal-induced apoptosis is dependent on the suppression of c-FLIPL expression via down-regulation of p65 in endothelial cells. J Cell Mol Med. 2017;21:2720–2731.
    1. Galkina E, Ley K. Immune and inflammatory mechanisms of atherosclerosis (*). Annu Rev Immunol. 2009;27:165–197.

MeSH terms