Possible causes of atherosclerosis: lncRNA COLCA1 induces oxidative stress in human coronary artery endothelial cells and impairs wound healing

Abstract

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 COLCA1 (colorectal cancer associated 1)/hsa-miR-371a-5p/SPP1 (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 COLCA1 in HCAECs was performed by siRNA interference technology to verify the role of COLCA1 in the biological function changes of HCAECs after oxLDL stimulation, and further prove that COLCA1 affects SPP1 through hsa-miR-371a-5p.Results: OxLDL can affect the oxidative stress response of HCAECs, which in turn affects the apoptosis and wound healing ability of HCAECs. COLCA1 and SPP1 were highly expressed after oxLDL stimulation, while hsa-miR-371a-5p was the opposite. After COLCA1 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 COLCA1 interference and recovery of the expression of hsa-miR-371a-5p, these improved functions disappeared. The dual-luciferase assay confirmed that hsa-miR-371a-5p and COLCA1, hsa-miR-371a-5p and SPP1 has binding targets.Conclusions: OxLDL can up-regulate the expression of COLCA1 in HCAECs, which in turn affects the intracellular COLCA1/hsa-miR-371a-5p/SPP1 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.

Construction of an oxidative stress-related lncRNAs signature to predict prognosis and the immune response in gastric cancer

“…Therefore, we presumed that the high expression of ARRDC1-AS1 in GC indicates its role as a tumor suppressor. In another study of coronary artery endothelial cells, the high expression of COLCA1 was stimulated by oxidized low-density lipoprotein, which regulates the level of oxidative stress in cells, thus leading to a sustained inflammatory response in cells 38 . This was consistent with the high expression of COLCA1 in our experiment.…”

Higher gestational weight gain delays wound healing and reduces expression of long non‐coding RNA KLRK1‐AS1 in neonatal endothelial progenitor cells

“…MEG3 , is involved. In fact, the role of lncRNAs in endothelial dysfunction associated with metabolic derangements is not surprising due to their involvement in inflammation and oxidative stress (Li et al., 2022 ; Pant et al., 2023 ; Zhou et al., 2020 ).…”

Differentially Expressed Genes Analysis in the Human Small Airway Epithelium of Healthy Smokers Shows Potential Risks of Disease Caused by Oxidative Stress and Inflammation and the Potentiality of Astaxanthin as an Anti-Inflammatory Agent

“…Inhibition of HDAC2 is known to prevent infammatory disorders and ROS production in EPCs with high glucose levels [35]. SPP1 is highly expressed after stimulation of oxidized low-density lipoprotein (oxLDL) and plays a role in causing infammation of human coronary artery endothelial cells (HCAECs) [36]. High TKT expression is also associated with advanced tumor stage and TKT inhibitors promote apoptosis of lung adenocarcinoma cells and cell cycle blockade [37].…”