1. TNF-α regulates apoptosis of human vascular smooth muscle cells through gap junctions
- Author
-
Jun Fang and Mei Tang
- Subjects
0301 basic medicine ,Cancer Research ,Vascular smooth muscle ,Myocytes, Smooth Muscle ,Cell ,Gene Expression ,Apoptosis ,030204 cardiovascular system & hematology ,Biology ,Biochemistry ,Muscle, Smooth, Vascular ,Proinflammatory cytokine ,03 medical and health sciences ,0302 clinical medicine ,Genetics ,medicine ,Humans ,Myocyte ,Molecular Biology ,Cells, Cultured ,Cell Proliferation ,Oncogene ,Caspase 3 ,Tumor Necrosis Factor-alpha ,Kinase ,JNK Mitogen-Activated Protein Kinases ,Gap Junctions ,musculoskeletal system ,Cell biology ,030104 developmental biology ,medicine.anatomical_structure ,Gene Expression Regulation ,Oncology ,Connexin 43 ,cardiovascular system ,Cancer research ,Cytokines ,Molecular Medicine ,Tumor necrosis factor alpha ,sense organs ,Signal Transduction - Abstract
Inflammatory cytokines are released by immune cells and are able to induce vascular smooth muscle cells (VSMCs) to undergo apoptosis, causing atherosclerotic plaque rupture. Changes in the expression levels of connexins (Cxs) have been demonstrated in VSMCs to be involved in the pathogenesis of atherosclerotic progression. The present study examined the effect of tumor necrosis factor‑α (TNF‑α) on Cx43 expression levels and apoptosis in human VSMCs. Overexpression of Cx43 plasmids notably stimulated VSMC proliferation. TNF‑α directly inhibited Cx43 expression levels in a dose‑ and time‑dependent manner in VSMCs, however this was blocked by c‑Jun N‑terminal kinase inhibitor. TNF‑α also increased caspase‑3 activity and apoptosis of VSMCs through the inhibition of Cx43. These data suggested that TNF‑α induced the apoptosis of VMSCs and prompted the destabilization of atherosclerotic plaques by downregulating Cx43.
- Published
- 2017