BACKGROUND: Atherosclerosis remains a leading cause of cardiology disease worldwide, which vascular smooth muscle cells (VSMCs) proliferation and apoptosis are involved. Increasing evidences have revealed that long non-coding RNAs (lncRNAs) considered to be critical regulatory factors of VSMCs function. However, the molecular mechanism is not fully understood. METHODS: First, we establish the ox-LDL induced VSMC model. We conducted RT-PCR to measure MEG3 expression and miR-361-5p expression in this model. The proliferation and apoptosis of VSMCs were measured via CCK-8 proliferative assay and flow cytometry respectively. We used knockdown and overexpression system to identify the molecular mechanism. In addition, luciferase report assay and bioinformatics analysis were used to confirm the bio-target of different factors. RESULTS: LncRNA MEG3 was down-regulated and related with miR-361-5p expression in ox-LDL injured VSMCs. Inhibition of lncRNA MEG3 promotes the proliferation and decelerates apoptosis of VSMCs. Moreover, MEG3 acts as a competing endogenous RNA (ceRNA) for miR-361-5p and further regulate ABCA1 expression regulate proliferation and apoptosis in ox-LDL injured VSMCs. CONCLUSION: These results suggest that LncRNA MEG3 regulate proliferation and apoptosis in ox-LDL injured VSMCs and function as a ceRNA for miR-361-5p to modulate ABCA1 expression.
BACKGROUND:Atherosclerosis remains a leading cause of cardiology disease worldwide, which vascular smooth muscle cells (VSMCs) proliferation and apoptosis are involved. Increasing evidences have revealed that long non-coding RNAs (lncRNAs) considered to be critical regulatory factors of VSMCs function. However, the molecular mechanism is not fully understood. METHODS: First, we establish the ox-LDL induced VSMC model. We conducted RT-PCR to measure MEG3 expression and miR-361-5p expression in this model. The proliferation and apoptosis of VSMCs were measured via CCK-8 proliferative assay and flow cytometry respectively. We used knockdown and overexpression system to identify the molecular mechanism. In addition, luciferase report assay and bioinformatics analysis were used to confirm the bio-target of different factors. RESULTS: LncRNA MEG3 was down-regulated and related with miR-361-5p expression in ox-LDL injured VSMCs. Inhibition of lncRNA MEG3 promotes the proliferation and decelerates apoptosis of VSMCs. Moreover, MEG3 acts as a competing endogenous RNA (ceRNA) for miR-361-5p and further regulate ABCA1 expression regulate proliferation and apoptosis in ox-LDL injured VSMCs. CONCLUSION: These results suggest that LncRNA MEG3 regulate proliferation and apoptosis in ox-LDL injured VSMCs and function as a ceRNA for miR-361-5p to modulate ABCA1 expression.
Authors: Alexandra V Rozhkova; Veronika G Dmitrieva; Elena V Nosova; Alexander D Dergunov; Svetlana A Limborska; Liudmila V Dergunova Journal: J Cardiovasc Dev Dis Date: 2021-12-02