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© 1995 Oxford University Press

research-article

Inhibition of gap junctional intercellular communication between primary human smooth muscle cells by tumor necrosis factor {alpha}

Anne Mensink 3, Laura H.J.de Haan, Catriona M.M. Lakemond 1, Carin A. Koelman 2 and Jan H. Koeman

Department of Toxicology, Agricultural University Wageningen PO Box 8000, 6700 EA Wageningen, The Netherlands
1Present address: Centre for Protein Technology TNO/WAU, PO Box 8129, 6700 EU Wageningen, The Netherlands
2Present address: Immunohaematology and Blood Bank, Rijnsburgerweg 10, E3-Q, 2333 AA Leiden, The Netherlands

3To whom correspondence should be addressed

Tumor necrosis factor {alpha} (TNF{alpha}), a pleiotrophic cytokine present in atherosclerotic lesions, caused a dose-dependent and persistent reduction in gap junctional intercellular communication (GJIC) between primary human smooth muscle cells in vitro. A continuous presence of TNF{alpha} was required for this persistent inhibition. Pretreatment of smooth muscle cells with ascorbic acid, {alpha}-tocopherol or glutathione prevented this inhibition of GJIC by TNF{alpha}. The persistent blockage of GJIC by continuous exposure to TNF{alpha} suggests that TNFa may share some mechanistic similarities with exogenous tumor promoters. Furthermore, this reduction in GJIC by TNFa may provide an additional link between the processes of atherosclerosis and carcinogenesis. The protection afforded by antioxidant compounds suggests a role for active oxygen species in the promotion stage of atherosclerosis.


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