Journal
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
Volume 295, Issue 2, Pages C324-C331Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpcell.90622.2007
Keywords
smooth muscle; intermediate filaments; transgenic mice; hypertrophy
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Funding
- Swedish Research Council
- Medical Faculty Lund University
- Association Francaise contre les Myopathies
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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.
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