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MUSCLE CELL BIOLOGY AND CELL MOTILITY
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
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