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Merck
  • TNF‑α regulates apoptosis of human vascular smooth muscle cells through gap junctions.

TNF‑α regulates apoptosis of human vascular smooth muscle cells through gap junctions.

Molecular medicine reports (2017-01-12)
Mei Tang, Jun Fang
摘要

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.

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Sigma-Aldrich
抗-BrdU 抗体,小鼠单克隆抗体, clone BU-33, purified from hybridoma cell culture
Sigma-Aldrich
抗鼠 IgG(全分子)− 过氧化物酶 兔抗, IgG fraction of antiserum, buffered aqueous solution