Over expression of smooth muscle specific caldesmon by transfection and intermittent agonist induced contraction alters cellular morphology and restores differentiated smooth muscle phenotype.

Abstract excerpt

PURPOSE: The thin filament associated protein h-caldesmon (h-CaD) modulates actin myosin interaction and contraction. Bladder outlet obstruction and detrusor hypertrophy are associated with the over expression of the nonmuscle CaD isoform l-CaD. It implies a poorly differentiated state of bladder myocytes and cytoskeletal remodeling in detrusor hypertrophy. We determined if h-CaD expression can be increased in a...

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