Altered expression of thin filament‐associated proteins in hypertrophied urinary bladder smooth muscle

Neurourology and Urodynamics - Tập 25 Số 1 - Trang 78-88 - 2006
Anita Mannikarottu1,2, Michael E. DiSanto1, Stephen A. Zderic3, Alan J. Wein1, Samuel Chacko4,1
1Division of Urology, University of Pennsylvania, Philadelphia, Pennsylvania
2Dr. Mannikarottu is a trainee in the Urology Training grant T32-DK07708.
3Children's Hospital of Philadelphia, Philadelphia, Pennsylvania
4Division of Pathobiology, University of Pennsylvania, Philadelphia, Pennsylvania

Tóm tắt

AbstractAimsObstruction of the urinary bladder outlet induces detrusor smooth muscle (DSM) hypertrophy. The goal of this study was to determine whether the composition of thin filament‐associated proteins, known to play important roles in cytoskeletal structure and/or the regulation of contraction, is altered in DSM during hypertrophy.MethodsDSM hypertrophy was induced in male rabbits by partial ligation of the urethra. Sham‐operated rabbits served as a control. Reverse transcriptase‐polymerase chain reaction (RT‐PCR) and real‐time PCR revealed a significant increase in the expression of mRNAs for basic (h1) calponin (CaP), and α‐isoform of tropomyosin (Tm) in hypertrophied DSM compared to controls. Western blotting and two‐dimensional (2‐D) gel electrophoresis showed enhanced expression of these proteins and also a significant increase in the expression of β‐non muscle and γ‐smooth muscle actin in the DSM from obstructed bladders, while α‐actin remained constant.ResultsEnhanced expression of these proteins in the DSM from obstructed bladders was confirmed by immunofluorescence microscopy. Double immunostaining with Cap/Tm and α/β‐actin‐specific antibodies showed co‐localization of these proteins in myocytes. Colocalization of smooth muscle specific myosin and CaP to cytoplasmic filaments in cells dissociated from the hypertrophied DSM indicated that these cells are differentiated smooth muscle cells.ConclusionsThe change in the isoforms of actin, Cap, and Tm may be part of the molecular mechanism for bladder compensation in increased urethral resistance. Neurourol. Urodynam. © 2005 Wiley‐Liss, Inc.

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