Abstract
RATIONALE: Airway epithelial cells play a central role in the inflammatory, apoptotic, and remodeling processes associated with asthma. Within this context, a key function is exerted by transforming growth factor-beta (TGF-beta). Recent growing evidence suggests that chloride (Cl-) channels are critical to the cell apoptosis. We investigated how TGF-beta induce airway epithelial cells apoptosis via interfering with the volume-regulated chloride channel (ClC).
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