LncRNA OIP5-AS1 accelerates ox-LDL-treated HUVECs injury by NF-κB pathway via miR-30c-5p.

BACKGROUND: Oxidized low-density lipoprotein (ox-LDL) could induce endothelial injury and played a vital role in the progression and development of atherosclerosis. This study aimed to investigate the role of Opa-interacting protein 5 antisense RNA 1 (OIP5-AS1) in ox-LDL-induced human umbilical vascular endothelial cells (HUVECs) injury and the potential mechanisms. METHODS: Cell proliferation and apoptosis were evaluated by Cell Counting Kit-8 (CCK-8) assay and flow cytometry assay, respectively. The levels of lactate dehydrogenase (LDH), reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD) and nitric oxide (NO) were detected by corresponding detection kits, respectively. Quantitative real-time PCR (qRT-PCR) was conducted to measure the expression of OIP5-AS1 or microRNA-30c-5p (miR-30c-5p) in HUVECs. Binding between OIP5-AS1 and miR-30c-5p was predicted through bioinformatics analysis and confirmed by dual-luciferase reporter assay and RNA immunoprecipitation (RIP). Western blot was used to analyze p-IκB, IκB, p-p65 and p65 levels. RESULTS: In HUVECs, exposure to ox-LDL led to a decrease in cell viability and an increase in LDH release and apoptosis with concomitant enhancement of oxidative stress, as evidenced by increased ROS and MDA generation, as well as decreased SOD activity and NO levels, while OIP5-AS1 knockdown or miR-30c-5p upregulation could rescue these effects above. Mechanically, OIP5-AS1 functioned as a sponge of miR-30c-5p. OIP5-AS1-induced injury and apoptosis, oxidative stress and activation of NF-κB pathway were reversed by miR-30c-5p in ox-LDL-treated HUVECs. CONCLUSION: OIP5-AS1 contributed to ox-LDL-treated HUVECs injury by activation of NF-κB pathway via miR-30c-5p.

A comprehensive meta-analysis on relationship between CYP11B2 rs1799998 polymorphism and atrial fibrillation.

BACKGROUND: The correlation between CYP11B2 rs1799998 polymorphism and atrial fibrillation (AF) was analyzed by several studies, but the results of these studies were inconsistent. Thus, we performed this study to obtain a more conclusive result on relationship between CYP11B2 rs1799998 polymorphism and AF. METHODS: Eligible studies were searched in PubMed, Medline and Embase. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated to estimate the strength of correlation. RESULTS: A total of 12 studies with 5466 participants were analyzed. We found that CYP11B2 rs1799998 polymorphism was significantly associated with AF in overall population under recessive genetic model with FEM (P = 0.005, OR = 1.29, 95%CI 1.08-1.54), but no positive results were detected in overall analyses with REMs. Further subgroup analyses revealed that CYP11B2 rs1799998 polymorphism was significantly correlated with AF in East Asians, but not in West Asians. Furthermore, significant associations between rs1799998 polymorphism and AF were observed in subjects with essential hypertension (EH) and heart failure (HF). No any other positive results were found in overall and subgroup analyses. CONCLUSIONS: Overall, our meta-analysis suggested that rs1799998 polymorphism may serve as a potential biological marker of AF in East Asians and subjects with EH or HF.