CircRNA RSF1 regulated ox-LDL induced vascular endothelial cells proliferation, apoptosis and inflammation through modulating miR-135b-5p/HDAC1 axis in atherosclerosis

BACKGROUND: Atherosclerosis (AS) is the most common type in cardiovascular disease. Due to its complex pathogenesis, the exact etiology of AS is unclear. circRNA has been shown to play an essential role in most diseases. However, the underlying mechanism of circRNA in AS has been not understood clearly. METHODS: Quantitative Real-Time PCR assay was used to detect the expression of circRSF1, miR-135b-5p and histone deacetylase 1 (HDAC1). Western blot was applied to the measure of protein expression of HDAC1, B-cell lymphoma-2 (Bcl-2), BCL2-associated X (Bax), cleaved-caspase-3, vascular cell adhesion molecule 1 (VCAM1), intercellular cell adhesion molecule-1 (ICAM1) and E-selectin. MTT assay and flow cytometry were used to detect cell proliferation and apoptosis, respectively. Dual luciferase reporter assay and RIP assay was used to determine the relationship among circRSF1, miR-135b-5p and HDAC1. Besides, an ELISA assay was performed to measure the levels of IL-1ß, IL-6, TNF-α and IL-8. RESULTS: In this study, ox-LDL inhibited circRSF1 and HDAC1 expression while upregulated miR-135b-5p expression in Human umbilical vein endothelial cells (HUVECs). Importantly, ox-LDL could inhibit HUVECs growth. Moreover, promotion of circRSF1 or inhibition of miR-135b-5p induced cell proliferation while inhibited apoptosis and inflammation of ox-LDL-treated HUVECs, which was reversed by upregulating miR-135b-5p or downregulating HDCA1 in oxLDL-treated HUVECs. More than that, we verified that circRSF1 directly targeted miR-135b-5p and HDAC1 was a target mRNA of miR-135b-5p in HUVECs. CONCLUSION: CircRSF1 regulated ox-LDL-induced vascular endothelial cell proliferation, apoptosis and inflammation through modulating miR-135b-5p/HDAC1 axis in AS, providing new perspectives and methods for the treatment and diagnosis of AS.

Expression of apoptosis inducing factor and apoptosis of nervous cells in infectious brain injury rat models induced by pneumolysin and their significance / 中华神经医学杂志

Objective To explore the expression ofapoptosis inducing factor (AIF) and the apoptosis ofnervous cells in infectious brain injury rat models induced by pneumolysin (PLY) and their significance.Methods A total of 80 infant SD rats were randomly divided into normal saline treatment group (NS group,n=40) and PLY treatment group (PLY group,n=40).Each group was divided into 4 subgroups:NS observation subgroups at the 6,12,24 and 48 h of treatment and PLY observation subgroups at the 6,12,24 and 48 h of treatment (n=10).Five rats in these subgroups were injected with Evan' s blue (EB) to determine the damage of BBB by measuring the content of EB in the brain tissues;the other 5 rats in these subgroups were not given EB,and their brain tissues were obtained to detect the protein expressions of NSE,GFAP and AIF by immunohistochemistry,and their apoptosis was examined by TUNEL staining.Results As compared with those in the NS treatment subgroups,the brain EB content and the expression levels of NSE,GFAP and AIF in the PLY treatment subgroups were significantly higher,and the number of apoptotic cells was significantly increased (P＜0.05).The number of apoptotic cells was positively correlated to the protein expression level of AIF in the PLY treatment group (r=0.959,P=0.000).Conclusion Apoptosis plays a role in the formation and development of infectious brain injury of rats and AIF might involve in the apoptosis ofneurocyte.