MicroRNA-377 Alleviates Myocardial Injury Induced by Hypoxia/Reoxygenation via Downregulating LILRB2 Expression

Abstract

Background: miR-377 is closely related to myocardial regeneration. miR-377-adjusted mesenchymal stem cells abducted ischemic cardiac angiogenesis. Nevertheless, there were rarely reports about the impact of miR-377 on myocardial ischemia injury. The purpose of this work is that whether miR-377 can protect against myocardial injury caused by hypoxia/reoxygenation (H/R). Methods: Gene expression omnibus database ( http://www.ncbi.nlm.nih.gov/geo/ ; no. GSE53211) was utilized to study the differential expression of miR-377 in patients with an acute ST-segment elevation myocardial infarction and healthy controls. The luciferase activity was determined utilizing the dual-luciferase reporter system. Quantitative real-time polymerase chain reaction and Western blotting were used to measure the messenger RNA and protein level. Results: Low expression of miR-377 and high expression of leukocyte immunoglobulin-like receptor B2 (LILRB2) were identified in patients with myocardial infarction from analyzing the Gene Expression Omnibus data set. Besides, miR-377 expression was downregulated in cardiomyocyte exposed to H/R. Additionally, overexpression of miR-377 could visibly improve cardiomyocyte injury by regulating cell activity and apoptosis. Conclusions: In short, our findings suggested that miR-377/LILRB2 might regard as a hopeful therapeutic target for myocardial ischemic.

MiR-518a-5p Targets GZMB to Extenuate Vascular Endothelial Cell Injury Induced by Hypoxia-Reoxygenation and Thereby Improves Myocardial Ischemia

“…33) As mentioned in the article, the up-regulation of miR-377 could significantly improve myocardial cell injury by targeting LILRB2 to regulate cell activity and apoptosis. 34) In our research, the outcomes illustrated that the miR-518a-5p expression was significantly down-regulated in MI, and we confirmed that the up-regulation of miR-518a-5p weakened GZMB expression by targeting the 3'-UTR of GZMB mRNA. Besides, miR-518a-5p could promote cell proliferation and suppress apoptosis by targeting GZMB so as to ameliorate H/R-induced HUVEC injury.…”

Maternal High Fat Diet and Diabetes Disrupts Transcriptomic Pathways That Regulate Cardiac Metabolism and Cell Fate in Newborn Rat Hearts

“…When comparing HF diet exposed offspring to control samples, Rho family GTPase 1 (Rnd1), TNF receptor superfamily member 12A (Tnfrsf12a), heparin-binding EGF-like growth factor (Hbegf ) and a group of microRNAs, were discretely upregulated in addition to the aforementioned Fbln5. MicroRNAs are non-coding RNA, 19-24 nucleotides in length, that are known to regulate almost all biological processes, including glucose and lipid metabolism, apoptosis, signal transduction, and inflammatory responses (92). Specifically, mir323, mir539, mir377, and mir382 all demonstrate significant enrichment in samples taken from the HF diet groups.…”

“…In rat models of myocardial infarction, mir539 expression increases significantly and binds to and inhibits the expression of MEK leading to impaired proliferation and apoptosis of cardiomyocytes ( 94 ). Mir377 also influences myocardial regeneration and angiogenesis by targeting many genes involved in inflammation, oxidative stress, and angiogenesis; converse to mir539 , it mitigates myocardial injury following ischemia-reperfusion injury by inducing angiogenesis and stem cell proliferation in ischemic myocardium ( 92 , 95 ). While no cardiac specific associations have been reported for mir382 , it has been observed to function as a PI3K/Akt pathway inhibitor ( 96 ) adding more relevance to network studies.…”

Knockdown of hsa_circ_0001275 reverses dexamethasone-induced osteoblast growth inhibition via mediation of miR-377/CDKN1B axis

“…In the current study, hsa_circ_0001275 could sponge miR-377 in hFOB1.19 cells. Previous reports have confirmed that miR-377 participates in the development of various types of diseases [30,31]. In addition, miR-377 was reported to be involved in the dysfunction of osteoblasts [32,33].…”