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Am J Physiol Cell Physiol 295: C324-C331, 2008. First published June 18, 2008; doi:10.1152/ajpcell.90622.2007
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MUSCLE CELL BIOLOGY AND CELL MOTILITY

Role of desmin in active force transmission and maintenance of structure during growth of urinary bladder

R. Sjuve Scott,2 Z. Li,3 D. Paulin,4 B. Uvelius,2 J. V. Small,5 and A. Arner1

1Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm; 2Department of Urology, Lund University, Lund, Sweden; 3Laboratory of Physiology and Physiopathology, UMR7079-Centre National de la Recherche Scientifique, Pierre and Marie Curie University; 4Laboratoire de Biologie Moléculaire de la Différentiation, Paris VII University, Paris, France; and 5Institute of Molecular Biotechnology, Austrian Academy of Sciences, Vienna, Austria

Submitted 12 December 2007 ; accepted in final form 12 June 2008

Role of the intermediate filament protein desmin in hypertrophy of smooth muscle was examined in desmin-deficient mice (Des–/–). A partial obstruction of the urethra was created, and after 9–19 days bladder weight increased approximately threefold in both Des–/– and wild type (Des+/+) animals. Bladder growth was associated with the synthesis of actin and myosin. In the hypertrophic Des+/+ bladder, the relative content of desmin increased. In Des–/–mice, desmin was absent. No alterations in the amount of vimentin were observed. Although Des–/– obstructed bladders were capable of growth, they had structural changes with a partial disruption of the wall. Des–/–bladders had slightly lower passive stress and significantly lower active stress compared with Des+/+. Des–/–preparations had lower shortening velocity. During hypertrophy, these structural and mechanical alterations in the Des–/–urinary bladder became more pronounced. In conclusion, desmin in the bladder smooth muscle is not needed for growth but has a role in active force transmission and maintenance of wall structure.

smooth muscle; intermediate filaments; transgenic mice; hypertrophy



Address for reprint requests and other correspondence: A. Arner, Dept. of Physiology and Pharmacology, Karolinska Institutet, v Eulers v 8, SE 171 77 Stockholm, Sweden (e-mail: Anders.Arner{at}ki.se)







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