AI Article Synopsis
- - The study explores the role of intronic microRNA-28 (miR-28) and its host gene, LIM domain lipoma-preferred partner (LPP), in promoting smooth muscle cell migration related to atherosclerosis.
- - Researchers aimed to validate how miR-28-5p inhibits ERK2 and its impact on atherosclerosis and cardiovascular health, using various scientific analysis methods.
- - Findings revealed that miR-28-5p enhances the expression of ATP-binding cassette transporter A1 (ABCA1) by inhibiting ERK2, and higher plasma levels of miR-28-5p correlate with increased high-density lipoprotein cholesterol in patients with unstable angina.
Article Abstract
The biological function of the intronic microRNA-28 (miR-28) may be associated with the biological roles of its host gene, LIM domain lipoma‑preferred partner (LPP). LPP has been reported to promote smooth muscle cell migration in arterial injury and atherosclerosis. However, the mechanism of miR‑28 in atherosclerosis remains unclear. In the current study, the aim was to validate the inhibitory effect of miR‑28‑5p on extracellular signal‑regulated kinase 2 (ERK2), to investigate its biological role in atherosclerosis and its association with cardiovascular disease. Western blotting and stem‑loop reverse transcription‑quantitative polymerase chain reaction combined with TaqMAN microRNA analysis was conducted. The current study demonstrated that miR‑28‑5p upregulated the expression of ATP‑binding cassette transporter A1 (ABCA1) via the inhibition of ERK2 in HepG2 cells. In addition, increased levels of plasma miR‑28‑5p were positively correlated with the levels of high‑density lipoprotein cholesterol in patients with unstable angina. This suggests that miR-28-5p participates in atherosclerosis via ERK2-mediated upregulation of the ABCA1 pathway.
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| http://dx.doi.org/10.3892/mmr.2015.4563 | DOI Listing |
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