Effect of dual mTOR inhibitor on TGFβ1-induced fibrosis in primary human urethral scar fibroblasts

Biomed Pharmacother. 2018 Oct:106:1182-1187. doi: 10.1016/j.biopha.2018.07.070. Epub 2018 Jul 18.

Abstract

Background: TGFβ1 and mTOR are considered to play important roles in fibrotic diseases. Rapamycin has been reported to inhibit urethral stricture formation in a rabbit model of urethral fibrosis.

Aim: To evaluate if dual mTOR inhibitor has a superior efficacy compared with rapamycin on inhibiting cell proliferation and collagen expression in human urethral scar fibroblasts (HUSFs).

Methods: We established HUSF cultures from fresh surgical specimen. The HUSFs were identified with typical fibroblast markers using immunofluorescence. Then we examined the effect of TGFβ1 on HUSFs using Cell Counting Kit-8 and Western blot. The inhibiting effects of OSI-027 (a dual mTOR inhibitor) on cell proliferation and collagen expression in TGFβ1-induced HUSFs were compared with rapamycin using Cell Counting Kit-8, Western blot, and quantitative reverse transcriptase polymerase chain reaction (qRT-PCR).

Results: HUSFs were stained positive for vimentin, collagen I, and collagen III. TGFβ1 had no effect on cell proliferation but increased collagen I and collagen III expressions in HUSFs. OSI-027 was more effective inhibiting cell proliferation and collagen expression compared with rapamycin in TGFβ1-induced HUSFs. OSI-027 played a more important role in inhibiting TGFβ1-induced mTOR pathway and phosphorylation of Smad2 compared with rapamycin in HUSFs.

Conclusion: OSI-027 can inhibit the pro-fibrotic effects of TGFβ1 significantly compared with rapamycin in HUSFs. These findings may provide a new therapy in the adjunctive treatment of urethral stricture disease.

Keywords: Human urethral scar fibroblast; OSI-027; Rapamycin; TGFβ1; Urethral stricture.

MeSH terms

  • Cell Proliferation / drug effects
  • Cells, Cultured
  • Cicatrix / drug therapy*
  • Cicatrix / enzymology
  • Cicatrix / pathology
  • Collagen Type I / metabolism
  • Collagen Type I, alpha 1 Chain
  • Collagen Type III / metabolism
  • Dose-Response Relationship, Drug
  • Fibroblasts / drug effects*
  • Fibroblasts / enzymology
  • Fibroblasts / pathology
  • Fibrosis
  • Humans
  • Imidazoles / pharmacology*
  • Phosphorylation
  • Primary Cell Culture
  • Protein Kinase Inhibitors / pharmacology*
  • Signal Transduction
  • Sirolimus / pharmacology*
  • Smad2 Protein / metabolism
  • TOR Serine-Threonine Kinases / antagonists & inhibitors*
  • TOR Serine-Threonine Kinases / metabolism
  • Time Factors
  • Transforming Growth Factor beta1 / pharmacology*
  • Triazines / pharmacology*
  • Urethra / drug effects*
  • Urethra / enzymology
  • Urethra / pathology
  • Vimentin / metabolism

Substances

  • COL1A2 protein, human
  • COL3A1 protein, human
  • Collagen Type I
  • Collagen Type I, alpha 1 Chain
  • Collagen Type III
  • Imidazoles
  • OSI 027
  • Protein Kinase Inhibitors
  • SMAD2 protein, human
  • Smad2 Protein
  • Transforming Growth Factor beta1
  • Triazines
  • Vimentin
  • MTOR protein, human
  • TOR Serine-Threonine Kinases
  • Sirolimus