title: Modulation of phenotype of human prostatic stromal cells by transforming growth factor-betas.
abstract: BACKGROUND
  We investigated the effects of transforming growth factor (TGF)-betas on morphological and receptor phenotypes, as well as proliferation of four currently established human prostatic myofibroblast cell lines and one commercially available prostatic stromal cell line.
  
  
  METHODS
  The effects of TGF-betas on morphological changes and proliferation of the cells were studied by immunohistochemistry and bromodeoxyuridine assay, respectively. The expression of alpha 1-receptor subtypes was measured by real time quantitative reverse transcription-polymerase chain reaction (RT-PCR) and the radioligand binding assay for the receptors was also performed.
  
  
  RESULTS
  TGF-betas 1, 2, and 3 induced expression of desmin and myosin of cells of the established cell lines, and significantly inhibited their growth. The alpha 1a-receptor was expressed only in the commercially available cell line and alpha 1b and 1d, in all cell lines. TGF-beta 1 suppressed the expression of all three subtypes of the alpha 1-receptor. The binding sites of cells of all the cell lines were reduced by treatment with this growth factor.
  
  
  CONCLUSIONS
  TGF-betas may induce human prostatic stromal cells to express the smooth muscle phenotype and inhibited their growth. However, the growth factor reduced the binding sites of the receptor and suppressed mRNA expression of its subtypes, suggesting that morphological and receptor phenotypes may be regulated via more than one pathway by TGF-beta(s).
authors.affiliation: Department of Urology, Sapporo Medical University, Sapporo, Japan.
authors.forename: Toshihiro
authors.initials: T
authors.lastname: Hisataki
authors.forename: Naoki
authors.initials: N
authors.lastname: Itoh
authors.forename: Kazuhiro
authors.initials: K
authors.lastname: Suzuki
authors.forename: Atsushi
authors.initials: A
authors.lastname: Takahashi
authors.forename: Naoya
authors.initials: N
authors.lastname: Masumori
authors.forename: Noritsugu
authors.initials: N
authors.lastname: Tohse
authors.forename: Yuki
authors.initials: Y
authors.lastname: Ohmori
authors.forename: Shizuo
authors.initials: S
authors.lastname: Yamada
authors.forename: Taiji
authors.initials: T
authors.lastname: Tsukamoto
mesh_terms: D002455:Cell Division; D002460:Cell Line; D003893:Desmin / Q000096:biosynthesis; D005786:Gene Expression Regulation; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D009130:Muscle, Smooth / Q000166:cytology*; D009218:Myosins / Q000096:biosynthesis; D010641:Phenotype; D011467:Prostate / Q000166:cytology* / Q000473:pathology*; D011470:Prostatic Hyperplasia / Q000503:physiopathology*; D011471:Prostatic Neoplasms / Q000503:physiopathology*; D012333:RNA, Messenger / Q000096:biosynthesis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D017154:Stromal Cells; D016212:Transforming Growth Factor beta / Q000494:pharmacology; D053773:Transforming Growth Factor beta1; D053781:Transforming Growth Factor beta2; D053782:Transforming Growth Factor beta3
chemical_list: D003893:Desmin; D012333:RNA, Messenger; C508960:TGFB1 protein, human; C509041:TGFB2 protein, human; D016212:Transforming Growth Factor beta; D053773:Transforming Growth Factor beta1; D053781:Transforming Growth Factor beta2; D053782:Transforming Growth Factor beta3; D009218:Myosins