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The Journal of Neuroscience, January 15, 2003, 23(2):430-441

Connexin Mediates Gap Junction-Independent Resistance to Cellular Injury

Jane H.-C. Lin¹, Jay Yang³, Shujun Liu², Takahiro Takano², Xiaohai Wang², Qun Gao², Klaus Willecke⁴, and Maiken Nedergaard²

Departments of ¹ Pathology and ² Anatomy and Cell Biology, New York Medical College, Valhalla, New York 10595, ³ Department of Anesthesia, Columbia University College of Physicians and Surgeons, New York, New York 10032, and ⁴ Institut für Genetik, Abteilung Molekulargenetik, University of Bonn, 53117 Bonn, Germany

Although gap junctions regulate essential processes during development and differentiation, the role of gap junctions in cell death is poorly understood. We demonstrate here that the forced expression of connexin 43 (Cx43), the main constituent of astrocytic gap junctions, protected against cell injury with a potency that was comparable with that from the expression of the proto-oncogene bcl2. The expression of two other members of the Cx family, Cx32 and Cx40, also increased the resistance to injury from exposures to calcium overload, oxidative stress, metabolic inhibition, tamoxifen, and UV irradiation, but not against staurosporine- and dexamethasone-mediated death. Surprisingly, the anti-death activity of connexin proteins was independent of gap junction channel function, because physical isolation or the pharmacological inhibition of coupling did not significantly increase cell death. Moreover, cells expressing nonfunctional mutant connexins also acquired a high resistance to injury. These observations identify Cx proteins as active players in cell survival.

Key words: adhesion; C6 glioma; calcium homeostasis; hemichannels; cell morphology; purinergic receptors

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Copyright © 2003 Society for Neuroscience  0270-6474/03/232430-12$05.00/0

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