MicroRNA-130a-3p (miR-130a-3p) has been reported as closely related to atherosclerosis (AS). This study is to survey the effects of miR-130a-3p in endothelial cells (ECs) treated with oxidized low-density lipoprotein (ox-LDL) and explore underlying mechanisms. The proliferation and apoptosis of ox-LDL-treated HUVEC cells were determined by CCK-8, EdU, and flow cytometry assays. ELISA and Western blot analysis measured the expressions of cytokines and protein levels. Bioinformatics and dual-luciferase reporter assay were performed to predict and confirm that Mitogen-activated protein kinase 8 (MAPK8) was a direct target of miR-130a-3p, and MAPK8 was negatively associated with miR-130a-3p. As expected, miR-130a-3p was down-regulated in ox-LDL-treated HUVEC cells, and up-regulation of miR-130a-3p promoted proliferation and inhibited apoptosis of ox-LDL-treated HUVEC cells. Furthermore, miR-130a-3p mimics suppressed the expressions of TNF-α and IL-6 and decreased the protein levels of VCAM-1, ICAM-1 and E-selectin. MAPK8 was highly expressed in ox-LDL-treated HUVEC cells, and silence of MAPK8 promoted proliferation inhibited apoptosis, suppressed inflammatory responses, and decreased the levels of VCAM-1, ICAM-1, and E-selectin, over-expression of MAPK8 partially restored the functional effects of miR-130a-3p on proliferation, inflammatory responses, and the expressions of VCAM-1, ICAM-1 and E-selectin. This study indicates that miR-130a-3p may emerge as an effective target for treating AS.
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http://dx.doi.org/10.1016/j.heliyon.2024.e24541 | DOI Listing |
Cardiovasc Ther
January 2025
Department of Cardiovascular Medicine, Third Hospital of Shanxi Medical University, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Tongji Shanxi Hospital, Taiyuan, Shanxi Province 030032, China.
This research is aimed at unravelling the intricate relationship between transient receptor potential vanilloid 6 (TRPV6), protein kinase A (PKA), uncoupling protein 2 (UCP2), and atherosclerosis. By shedding light on the role of the TRPV6/PKA/UCP2 pathway in inhibiting inflammatory response and cell apoptosis in coronary atherosclerotic plaques, this study provides valuable insights into potential therapeutic targets for treating coronary artery disease (CAD). We established animal and cell models of atherosclerosis.
View Article and Find Full Text PDFPeerJ
November 2024
Hengyang Medical School, University of South China, The First Affiliated Hospital, Department of Cardiology, Hengyang, Hunan, China.
PeerJ
September 2024
Department of Neonatology, Renmin Hospital of Wuhan University, Wuhan, China.
Background: This study aims to identify a novel gene signature for coronary artery disease (CAD), explore the role of immune cell infiltration in CAD pathogenesis, and assess the cell function of mast cell-expressed membrane protein 1 () in human umbilical vein endothelial cells (HUVECs) treated with oxidized low-density lipoprotein (ox-LDL).
Methods: To identify differentially expressed genes (DEGs) of CAD, datasets GSE24519 and GSE61145 were downloaded from the Gene Expression Omnibus (GEO) database using the R "limma" package with < 0.05 and |log2 FC| > 1.
Hereditas
September 2024
Department of Respiratory and Critical Care Medicine, Zibo Central Hospital, No. 54, Gongqingtuan West Road, Zhangdian District, Zibo, 255020, Shandong, China.
Background: Acute pulmonary embolism (APE) is a major type of venous thromboembolism (VTE) with a high risk of mortality and disability. There is a lack of biomarkers for APE to indicate deteriorating development and predict adverse outcomes. This study evaluated the significance of miR-150-5p in APE aiming to explore a novel potential biomarker for APE.
View Article and Find Full Text PDFHeliyon
June 2024
The Third Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang, 310005, China.
Background: Endothelial dysfunction is the early stage of carotid atherosclerosis (CAS) in patients with hypertension. It is worth identifying the potential hub genes of endothelial dysfunction to elucidate pathological mechanism in the progression of the disease.
Method: We obtained gene expression profiles of GSE43292 from the Gene Expression Omnibus (GEO) database.
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