Exosomal long non-coding RNA LIPCAR derived from oxLDL-treated THP-1 cells regulates the proliferation of human umbilical vein endothelial cells and human vascular smooth muscle cells

Background: It has been reported that long non-coding RNA (lncRNA) LIPCAR is involved in the progression of atherosclerosis. However, the mechanism underlying the effects of LIPCAR on regulating the occurrence and development of atherosclerosis remains unclear. Methods: Reverse transcription-quantitative PCR was performed to detect the levels of LIPCAR in the plasma of patients with atherosclerosis and in THP-1 macrophages. THP-1 cells were stimulated with oxidized low-density lipoprotein (ox-LDL) to induce foam cell formation. Furthermore, Transwell assay was carried out to evaluate the migration ability of vascular smooth muscle cells (VSMCs). Results: The expression of LIPCAR in the plasma of patients with atherosclerosis was significantly higher compared with that in healthy subjects, while LIPCAR knockdown notably reversed ox-LDL-induced THP1 cell apoptosis. In addition, LIPCAR was upregulated in exosomes derived from THP-1 cells treated with ox-LDL (THP-1/ox-LDL Exo). Furthermore, THP-1/ox-LDL Exo significantly increased the expression levels of CDK2 and proliferative cell nuclear antigen in human VSMCs, while these effects were reversed following LIPCAR silencing. Conclusion: The results of the present study suggested that exosomal lncRNA LIPCAR derived from oxLDL modified THP-1 cells could promote the progression of atherosclerosis. Therefore, LIPCAR may be considered as a novel biomarker for the development of new strategies to treat atherosclerosis. (c) 2021 Elsevier Inc. All rights reserved.