title: Expression of parathyroid hormone/parathyroid hormone-related peptide receptor 1 in normal and diseased bladder detrusor muscles: a clinico-pathological study.
abstract: BACKGROUND
  To investigate the expression of parathyroid hormone (PTH)/PTH-related peptide (PTHrP) receptor 1 (PTH1R) in clinical specimens of normal and diseased bladders. PTHrP is a unique stretch-induced endogenous detrusor relaxant that functions via PTH1R. We hypothesized that suppression of this axis could be involved in the pathogenesis of bladder disease.
  
  
  METHODS
  PTH1R expression in clinical samples was examined by immunohistochemistry. Normal kidney tissue from a patient with renal cancer and bladder specimens from patients undergoing ureteral reimplantation for vesicoureteral reflux or partial cystectomy for urachal cyst were examined as normal control organs. These were compared with 13 diseased bladder specimens from patients undergoing bladder augmentation. The augmentation patients ranged from 8 to 31 years old (median 15 years), including 9 males and 4 females. Seven patients had spinal disorders, 3 had posterior urethral valves and 3 non-neurogenic neurogenic bladders (Hinman syndrome).
  
  
  RESULTS
  Renal tubules, detrusor muscle and blood vessels in normal control bladders stained positive for PTH1R. According to preoperative urodynamic studies of augmentation patients, the median percent bladder capacity compared with the age-standard was 43.6% (range 1.5-86.6%), median intravesical pressure at maximal capacity was 30 cmH2O (range 10-107 cmH2O), and median compliance was 3.93 ml/cmH2O (range 0.05-30.3 ml/cmH2O). Detrusor overactivity was observed in five cases (38.5%). All augmented bladders showed negative stainings in PTH1R expression in the detrusor tissue, but positive staining of blood vessels in majority of the cases.
  
  
  CONCLUSIONS
  Downregulation of PTH1R may be involved in the pathogenesis of human end-stage bladder disease requiring augmentation.
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Nishikawa
authors.forename: Rie
authors.initials: R
authors.lastname: Yago
authors.forename: Yuichiro
authors.initials: Y
authors.lastname: Yamazaki
authors.forename: Hiromitsu
authors.initials: H
authors.lastname: Negoro
authors.forename: Mari
authors.initials: M
authors.lastname: Suzuki
authors.forename: Masaaki
authors.initials: M
authors.lastname: Imamura
authors.forename: Yoshinobu
authors.initials: Y
authors.lastname: Toda
authors.forename: Kazunari
authors.initials: K
authors.lastname: Tanabe
authors.forename: Osamu
authors.initials: O
authors.lastname: Ogawa
authors.affiliation: Department of Urology, Hyogo College of Medicine, Nishinomiya, Japan. aqui@hyo-med.ac.jp.
authors.forename: Akihiro
authors.initials: A
authors.lastname: Kanematsu
mesh_terms: D000293:Adolescent; D000328:Adult; D002648:Child; D015536:Down-Regulation; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D010281:Parathyroid Hormone / Q000378:metabolism*; D044168:Receptor, Parathyroid Hormone, Type 1 / Q000378:metabolism*; D001743:Urinary Bladder / Q000378:metabolism* / Q000503:physiopathology; D001745:Urinary Bladder Diseases / Q000378:metabolism* / Q000503:physiopathology; D014563:Urodynamics; D055815:Young Adult
chemical_list: D010281:Parathyroid Hormone; D044168:Receptor, Parathyroid Hormone, Type 1