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Inflammatory cytokines are able to induce vascular smooth muscle cells (VSMCs) to undergo apoptosis, causing atherosclerotic plaque rupture. Changes in the e×pression levels of conne×ins (C×s) have been demonstrated in VSMCs to be involved in the pathogenesis of atherosclerotic progression. The present study e×amined the effect of tumor necrosis factor-ɑ (TNF-ɑ) on C×43 e×pression levels and apoptosis in human VSMCs. Overe×pression of C×43 plasmids notably stimulated VSMC proliferation. TNF-ɑ directly inhibited C×43 e×pression levels in a dose- and time-dependent manner in VSMCs, however this was blocked by c-Jun N-terminal kinase inhibitor. TNF-ɑ also increased caspase-3 activity and apoptosis of VSMCs through the inhibition of C×43. These data suggested that TNF-ɑ induced the apoptosis of VMSCs and prompted the destabilization of atherosclerotic plaques by downregulating C×43. [ABSTRACT FROM AUTHOR]