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- Title
Down-Regulation of miR-327 Alleviates Ischemia/Reperfusion-Induced Myocardial Damage by Targeting RP105.
- Authors
Ying Yang; Jun Yang; Xiao-wen Liu; Jia-wang Ding; Song Li; Xin Guo; Chao-jun Yang; Zhi-xin Fan; Hui-bo Wang; Qi Li; Hui-min Wang; Jian Yang
- Abstract
Background/Aims: Micro RNAs (miRNAs) play a very important role in myocardial ischemia/ reperfusion injury (MIRI), including in inflammation, apoptosis, and angiogenesis. Previous studies have demonstrated up-regulation of miR-327 in renal ischemia/reperfusion injury and MIRI. Via TargetScan, we found RP105 is a possible target gene of miR-327; our previous studies have also confirmed that RP105 acted as a cardioprotective protein in MIRI by reducing inflammation. However, the regulatory effect of miR-327 on RP105 has not previously been proposed. In our study, we aimed to identify the regulatory effect of miR-327 on RP105 protein in MIRI rats. Methods: Sixty male Sprague-Dawley rats were randomly divided into five groups, which were pre-treated with saline (sham and ischemia/reperfusion group), adenovirus-expressing miR-327-RNAi (Ad-miR-327-i group), control (Ad-NC group), or primiR-327 (Ad-miR-327 group) treatments. Three d'ys later, the rat MIRI model was established by ischemia for 30 min, followed by reperfusion for 3 h. Myocardium and plasma were harvested and assessed. Results: miR-327 was increased by nearly 3-fold both in myocardium and plasma, which down-regulated RP105 in a 3'-untranslated region-dependent manner, and down-regulation of miR-327 via adenovirus transfection indirectly suppressed the TLR4/ TLR2-MyD88-NF-κB signaling axis activation via up-regulation of RP105, which subsequently resulted in reduced myocardial infarct size, attenuated cardiomyocyte destruction, and alleviated inflammation. In contrast, up-regulation of miR-327 induced the opposite effect.
- Subjects
MICRORNA; CORONARY disease; REPERFUSION injury; INFLAMMATION prevention; MYOCARDIAL infarction; HEART cells
- Publication
Cellular Physiology & Biochemistry (Karger AG), 2018, Vol 49, Issue 3, p1090
- ISSN
1015-8987
- Publication type
Article
- DOI
10.1159/000493288