MALAT1 affects atherosclerosis by regulating endothelial cell’s microautophagy

School of Information Engineering, Ocean University of China, Qingdao, Shandong 266000, China

^* Corresponding author. Email: zhangrunqi@stu.ouc.edu.cn

Abstract

Autophagy of vessels endothelial cells is the critical pathological process in atherosclerosis (AS). Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is a kind of long non-coding RNA (lncRNA) that regulates the autophagy of vessels endothelial cells, including microautophagy. However, the relationship between AS and MALAT1 is not completely understood, and microautophagy has been ignored. In this study, I designed the experiments to research the impact of MALAT1 in endothelial cells, which could regulate the progression of AS. In the present study, I design to establish the AS model mice with low MALAT1 level. The expression level of MALAT1 needs to be detected to verify the mouse model. Then, the intensity of microautophagy of endothelial cells of mouse model and normal mouse are detected by RT-qPCR, immunofluorescence assay, and observation directly with electron microscope. The atherosclerosis progression and plaque stability are detected by comparing the rations of macrophage/vascular smooth muscle cell and collagen/lipid. This paper only provides theoretical experiment design and possible results about how MALAT1 affects AS by regulating microautophagy of vascular endothelial cells (VECs) which needs additional research in the pathology of atherosclerosis. This paper provided the possibility that MALTA1 regulates the microautophagy in VECs and MALTA1 may be the target to cure AS.