Possible causes of atherosclerosis: lncRNA induces oxidative stress in human coronary artery endothelial cells and impairs wound healing.

BACKGROUND

Atherosclerosis is the most common cause of cardiovascular disease, accompanied by high mortality and poor prognosis. Low-density lipoprotein (LDL) and its oxidized form oxidized low-density lipoprotein (oxLDL) play an important role in atherosclerosis. This article will explore the role of the lncRNA (colorectal cancer associated 1)// (secreted phosphoprotein 1) pathway in oxLDL in causing human coronary artery endothelial cells (HCAECs) inflammation and related biological function changes.

METHODS

OxLDL was used to stimulate HCAECs. The inflammatory response and biological function changes of HCAECs were analyzed, total RNA-seq was performed on HCAECs before and after stimulation, and RT-Qpcr (real-time quantitative PCR) was used to verify the differential genes. Interference of the expression of in HCAECs was performed by siRNA interference technology to verify the role of in the biological function changes of HCAECs after oxLDL stimulation, and further prove that affects through .

RESULTS

OxLDL can affect the oxidative stress response of HCAECs, which in turn affects the apoptosis and wound healing ability of HCAECs. and were highly expressed after oxLDL stimulation, while was the opposite. After interference, the oxidative stress level of HCAECs stimulated by oxLDL decreased, the apoptosis level also significantly decreased, and the wound healing ability was enhanced. After simultaneous interference and recovery of the expression of , these improved functions disappeared. The dual-luciferase assay confirmed that and , and has binding targets.

CONCLUSIONS

OxLDL can up-regulate the expression of in HCAECs, which in turn affects the intracellular pathway to regulate the level of oxidative stress in cells. This in turn affects the level of apoptosis and wound healing ability, which causes cells to produce a continuous inflammatory response.