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

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.