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  • Title: The B[a]P-increased intercellular communication via translocation of connexin-43 into gap junctions reduces apoptosis.
    Author: Tekpli X, Rivedal E, Gorria M, Landvik NE, Rissel M, Dimanche-Boitrel MT, Baffet G, Holme JA, Lagadic-Gossmann D.
    Journal: Toxicol Appl Pharmacol; 2010 Jan 15; 242(2):231-40. PubMed ID: 19874837.
    Abstract:
    Gap junctions are channels in plasma membrane composed of proteins called connexins. These channels are organized in special domains between cells, and provide for direct gap junctional intercellular communication (GJIC), allowing diffusion of signalling molecules <1 kD. GJIC regulates cell homeostasis and notably the balance between proliferation, cell cycle arrest, cell survival and apoptosis. Here, we have investigated benzo[a]pyrene (B[a]P) effects on GJIC and on the subcellular localization of the major protein of gap junction: connexin-43 (Cx43). Our results showed that B[a]P increased GJIC between mouse hepatoma Hepa1c1c7 cells via translocation of Cx43 from Golgi apparatus and lipid rafts into gap junction plaques. Interestingly, inhibition of GJIC by chlordane or small interference RNA directed against Cx43 enhanced B[a]P-induced apoptosis in Hepa1c1c7 cells. The increased apoptosis caused by inhibition of GJIC appeared to be mediated by ERK/MAPK pathway. It is suggested that B[a]P could induce transfer of cell survival signal or dilute cell death signal via regulation of ERK/MAPK through GJIC.
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