Inhibition of miR-652-3p Regulates Lipid Metabolism and Inflammatory Cytokine Secretion of Macrophages to Alleviate Atherosclerosis by Improving TP53 Expression.

Purpose: The aim was to elucidate the regulatory function of miR-652-3p on lipid metabolism and inflammatory cytokine secretion of macrophages in atherosclerosis. Methods: miR-652-3p level in atherosclerosis patients, ox-LDL-treated macrophages, and their controls were monitored by Q-PCR. After ox-LDL treatment and miR-652-3p mimic, si-TP53 and their controls transfection, ELISA, and Q-PCR assays were used to detect IL-1ß, IL-6, and TNF-α levels. oil red O staining was processed to verify cholesterol accumulation. CE/TC and lipid metabolism were also detected. The protein levels of ABCA1, ABCG1, PPARα, CRT1, ADRP, and ALBP were detected by western blot assay. Based on the TargetScan database, the TP53 3'UTR region had complementary bases with miR-652-3p, which was also verified by dual-luciferase reporter gene assay. Finally, the regulation of miR-652-3p and TP53 was confirmed by rescue assay in atherosclerosis. Results: miR-652-3p is highly expressed in atherosclerosis, miR-652-3p inhibitor decreased IL-1ß, IL-6, and TNF-α expression after ox-LDL treatment. Knockdown of miR-652-3p reduces foam formation in ox-LDL-treated macrophages. miR-652-3p inhibitor ameliorates cholesterol accumulation and lipid metabolism disorder. miR-652-3p negatively regulated TP53 in atherosclerosis. Si-TP53 rescued the effect of miR-652 inhibitor in atherosclerosis. Conclusion: miR-652-3p regulates the lipid metabolism of macrophages to alleviate atherosclerosis by inhibiting TP53 expression. It might be a potential target for atherosclerosis treatment.

Changes and Diagnostic Significance of miR-542-3p Expression in Patients with Myocardial Infarction.

Acute myocardial infarction (AMI) is a heart lesion, that endangers the life safety of patients. This study focused on exploring the clinical effect of miR-542-3p on AMI and no-reflow after percutaneous coronary intervention (PCI). Serum samples were collected from 100 AMI emergency inpatients. The expression of miR-542-3p was quantified by qPCR. The predictive role of miR-542-3p was disclosed by plotting ROC curve. In addition, AMI subjects were cataloged into a group of no-reflow and normal reflow group. The risk factors of no-reflow were estimated by logistic regression analysis. In the serum samples of AMI patients, the level of miR-542-3p showed a pattern of decreasing. MiR-542-3p expression represented a high sensitivity and specificity of the prediction of AMI. A decrease of miR-542-3p content was revealed in AMI patients without reflow after PCI. Logistic regression results reflected that miR-542-3p was an independent biomarker for no-reflow. The declined miR-542-3p expression was a predictive marker for AMI and no-reflow in AMI patients.

Constructing sodium alginate/carboxymethyl chitosan coating capable of catalytically releasing NO or CO for improving the hemocompatibility and endothelialization of magnesium alloys.

Although significant progress in developing biodegradable magnesium alloy materials in cardiovascular stents has been achieved recently, they still face challenges such as rapid in vivo corrosion degradation, inferior blood compatibility, and limited re-endothelialization after the implantation. Hydrogel coating that can catalyze the liberation of gas signal molecules offers a good solution to alleviate the corrosion rate and enhance the biocompatibility of magnesium and its alloys. In this study, based on alkaline heat treatment and construction of polydopamine coating on the surface of magnesium alloy, sodium alginate/carboxymethyl chitosan (SA/CMCS) gel was simultaneously covalently grafted onto the surface to build a natural polymer hydrogel coating, and selenocystamine (SeCA) and CO release molecules (CORM-401) were respectively immobilized on the surface of the hydrogel coating to ameliorate the anticoagulant performance and accelerate endothelial cells (ECs) growth by catalyzing the release of endogenous gas signal molecules (NO or CO). The findings verified that the as-prepared hydrogel coating can catalyze the liberation of CO or NO and significantly improve the corrosion resistance of magnesium alloy. At the same time, owing to the excellent hydrophilicity of the hydrogel coating, the good anticoagulant property of sodium alginate, and the ability of CMCS to promote the ECs growth, the modified magnesium alloy could significantly improve the albumin adsorption while preventing the adsorption of fibrinogen, hence significantly augmenting the anticoagulant properties and promoting the ECs growth. Under the catalytic release of NO or CO, the released gas molecules further enhanced hemocompatibility and promoted endothelial cell (EC) growth and the expression of vascular endothelial growth factor (VEGF) and NO of ECs. Therefore, the bioactive coatings that can catalyze the release of NO or CO have potential applications in constructing surface bioactive coatings for magnesium alloy materials used for intravascular stents.