Author:
Scott R. Sjuve,Li Z.,Paulin D.,Uvelius B.,Small J. V.,Arner A.
Abstract
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.
Publisher
American Physiological Society
Cited by
15 articles.
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