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Basic fibroblast growth factor causes urinary bladder overactivity through gap junction generation in the smooth

Masaaki Imamura1, Hiromitsu Negoro, Akihiro Kanematsu

  • 1Department of Urology, Graduate School of Medicine, Institute for Frontier Medical Sciences, Kyoto University, Kyoto, 606-8507 Japan.

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Basic fibroblast growth factor (bFGF) increases bladder smooth muscle cell (BSMC) coupling via connexin 43, contributing to overactive bladder in bladder outlet obstruction (BOO) models.

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Area of Science:

  • Urology
  • Cell Biology
  • Physiology

Background:

  • Overactive bladder (OAB) is common, often linked to bladder outlet obstruction (BOO).
  • Increased bladder smooth muscle cell (BSMC) coupling via gap junctions is a suspected OAB mechanism in BOO.
  • The regulatory system for these gap junction changes remains unclear.

Purpose of the Study:

  • To investigate the roles of basic fibroblast growth factor (bFGF) and connexin 43 (Cx43) in BOO-induced bladder overactivity.
  • To elucidate the signaling pathway by which bFGF influences Cx43 expression and gap junction formation.

Main Methods:

  • Urethral constriction model in rats to induce BOO.
  • In vitro studies using cultured rat BSMC treated with bFGF.
  • In vivo studies using gelatin hydrogels releasing bFGF on rat bladders.
  • Measurement of bFGF and Cx43 levels, cholinergic agonist sensitivity, and cystometric analysis.

Main Results:

  • BOO increased bFGF and Cx43 levels in rat bladders.
  • bFGF treatment upregulated Cx43 in cultured BSMC via the ERK1/2 pathway.
  • In vivo bFGF administration induced Cx43 upregulation, gap junction formation, and detrusor overactivity.
  • Increased bladder muscle sensitivity to cholinergic agonists was observed and blocked by gap junction inhibition.

Conclusions:

  • bFGF from the urothelium may induce bladder hypersensitivity to acetylcholine.
  • This occurs through gap junction generation in smooth muscle, contributing to myogenic overactivity in obstructed bladders.