Tang Mei, Fang Jun
Infusion Preparation Center of Pharmacy Department, Xianning Central Hospital & The First Clinical Hospital of Hubei University of Science and Technology, Xianning, Hubei 437100, P.R. China.
Division of Nephrology, Department of Internal Medicine, Xianning Central Hospital & The First Clinical Hospital of Hubei University of Science and Technology, Xianning, Hubei 437100, P.R. China.
Mol Med Rep. 2017 Mar;15(3):1407-1411. doi: 10.3892/mmr.2017.6106. Epub 2017 Jan 5.
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.
