title: Altered distribution of interstitial cells in the guinea pig bladder following bladder outlet obstruction.
abstract: OBJECTIVE
  We investigated the effects of bladder outlet obstruction (BOO) on the distribution of interstitial cells (ICs) in the guinea-pig bladder.
  
  
  METHODS
  Bladder overactivity of BOO animals was validated with urodynamic studies. Immunohistochemical analyses for Kit and vimentin as markers for ICs were performed on both BOO and control bladders. Morphological and functional properties of detrusor smooth muscle (DSM) were examined with alpha-smooth muscle actin staining and intracellular recording, respectively. Electron microscopy was also carried out to characterize ultrastructural morphology of ICs.
  
  
  RESULTS
  Two weeks after surgery, BOO animals showed an increased voiding frequency and a reduced voiding volume. Filling cystometry demonstrated a frequent incidence of non-voiding contractions, a reduced interval between voiding contractions and an increased voiding pressure in BOO bladders. In BOO bladders, the thickness of suburothelial and subserosal connective tissue layers was increased, whilst that of detrusor smooth muscle (DSM) layer was less affected. Population of Kit or vimentin immunoreactive ICs was increased in subserosal layers, and their distribution was altered in suburotherial layer in BOO bladders. Neither alpha-actin immunoreactivity nor spontaneous electrical activity of DSM was altered in BOO bladders. ICs were characterized by their numerous mitochondria and caveolae, and had a close contact with each other and with neighboring DSM or nerves.
  
  
  CONCLUSIONS
  These results demonstrated the increased population of ICs in the BOO guinea-pig model for the first time, and suggest that the altered distribution of ICs may contribute to the pathophysiology of bladder overactivity.
authors.affiliation: Department of Nephro-urology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan. yasuekbt@med.nagoya-cu.ac.jp
authors.forename: Yasue
authors.initials: Y
authors.lastname: Kubota
authors.forename: Hikaru
authors.initials: H
authors.lastname: Hashitani
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Shirasawa
authors.forename: Yoshiyuki
authors.initials: Y
authors.lastname: Kojima
authors.forename: Shoichi
authors.initials: S
authors.lastname: Sasaki
authors.forename: Yoshio
authors.initials: Y
authors.lastname: Mabuchi
authors.forename: Tsuyoshi
authors.initials: T
authors.lastname: Soji
authors.forename: Hikaru
authors.initials: H
authors.lastname: Suzuki
authors.forename: Kenjiro
authors.initials: K
authors.lastname: Kohri
mesh_terms: D000199:Actins / Q000032:analysis; D000200:Action Potentials; D000818:Animals; D021941:Caveolae / Q000648:ultrastructure; D004195:Disease Models, Animal; D005260:Female; D006168:Guinea Pigs; D007150:Immunohistochemistry; D046529:Microscopy, Electron, Transmission; D008928:Mitochondria / Q000648:ultrastructure; D009119:Muscle Contraction; D009130:Muscle, Smooth / Q000737:chemistry / Q000473:pathology* / Q000503:physiopathology / Q000648:ultrastructure; D019009:Proto-Oncogene Proteins c-kit / Q000032:analysis; D001743:Urinary Bladder / Q000737:chemistry / Q000473:pathology* / Q000503:physiopathology / Q000648:ultrastructure; D001748:Urinary Bladder Neck Obstruction / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D014563:Urodynamics; D014746:Vimentin / Q000032:analysis
chemical_list: D000199:Actins; D014746:Vimentin; D019009:Proto-Oncogene Proteins c-kit