title: Alterations in caveolin expression and ultrastructure after bladder smooth muscle hypertrophy.
abstract: OBJECTIVE
  Partial bladder outlet obstruction in male rabbits causes detrusor smooth muscle hypertrophy and voiding dysfunction similar to that observed in men with benign prostate hyperplasia. Using this model, we analyzed the protein expression and ultrastructure of caveolae and the intermediate size filament in detrusor smooth muscle following partial bladder outlet obstruction induced hypertrophy.
  
  
  METHODS
  Detrusor smooth muscle sections from bladder body were processed for immunofluorescence and electron microscopy. Western analysis was performed to determine the expression of caveolin isoform-1, 2 and 3, and intermediate size filament proteins.
  
  
  RESULTS
  Detrusor smooth muscle cells from both normal and hypertrophied bladders contain orderly arrays of thick and thin myofilaments, interspersed with dense bodies. In addition, there was an increase in intermediate size filaments in the hypertrophic detrusor smooth muscle cells. The dense plaques in the inner membrane of hypertrophied detrusor smooth muscle were longer than those of the control. Detrusor smooth muscle from hypertrophied bladder revealed a decreased number of caveolae and a lack of their orderly distribution at the plasma membrane. Western blotting showed decreased expression of caveolin-1, 2 and 3 in hypertrophied detrusor smooth muscle.
  
  
  CONCLUSIONS
  Caveolae serve as platforms for proteins and receptors that have a role in signal transduction. The decreased number of caveolae and caveolin protein expression in hypertrophied detrusor smooth muscle might contribute to alterations in signal transduction pathways that regulate the downstream effects of agonist induced contraction, including calcium sensitization, observed in obstructed bladder. In addition, the increased number of intermediate size filaments in the hypertrophied detrusor smooth muscle is likely to alter the cytoskeletal structure and affect the cellular transmission of passive and/or active force.
authors.affiliation: Department of Pathobiology, University of Pennsylvania, Philadelphia, Pennsylvania 19036, USA.
authors.forename: Erzsébet
authors.initials: E
authors.lastname: Polyák
authors.forename: Ettickan
authors.initials: E
authors.lastname: Boopathi
authors.forename: Sunish
authors.initials: S
authors.lastname: Mohanan
authors.forename: Maoxian
authors.initials: M
authors.lastname: Deng
authors.forename: Stephen A
authors.initials: SA
authors.lastname: Zderic
authors.forename: Alan J
authors.initials: AJ
authors.lastname: Wein
authors.forename: Samuel
authors.initials: S
authors.lastname: Chacko
mesh_terms: D000818:Animals; D021941:Caveolae; D022461:Caveolins / Q000096:biosynthesis*; D006984:Hypertrophy; D066298:In Vitro Techniques; D008297:Male; D008854:Microscopy, Electron; D009130:Muscle, Smooth / Q000378:metabolism* / Q000473:pathology* / Q000648:ultrastructure; D011817:Rabbits; D001743:Urinary Bladder / Q000378:metabolism* / Q000473:pathology* / Q000648:ultrastructure
chemical_list: D022461:Caveolins