Basic fibroblast growth factor modulates proliferation and collagen expression in urinary bladder smooth muscle cells

Area of Science:

• Urology
• Cell Biology
• Biochemistry

Background:

• Bladder hypertrophy, common in clinical urologic diseases, involves smooth muscle hyperplasia and altered matrix composition.
• The specific roles of growth factors in bladder hypertrophy pathophysiology are not well understood.

Purpose of the Study:

• To investigate the role of basic fibroblast growth factor (bFGF) in bladder smooth muscle cell (BSMC) proliferation and extracellular matrix remodeling.
• To elucidate the signaling pathways involved in bFGF-mediated effects on BSMC.

Main Methods:

• Utilized a rat bladder smooth muscle cell (BSMC) culture system for in vitro studies.
• Developed an original animal model for in vivo bFGF release using a gelatin hydrogel.
• Induced bladder hypertrophy in rats via urethral constriction.

Main Results:

• bFGF treatment promoted BSMC proliferation both in vitro and in vivo.
• bFGF modulated collagen expression (downregulated type I, upregulated type III) and activated ERK1/2 signaling.
• In vivo, bFGF increased type III collagen and bladder contractile force; hypertrophied bladders showed increased urothelial bFGF and BSMC proliferation.

Conclusions:

• bFGF acts as a paracrine signal from the urothelium, stimulating BSMC proliferation and matrix production.
• bFGF contributes to the hypertrophic remodeling of the bladder smooth muscle layer.
• Targeting bFGF signaling may offer therapeutic potential for bladder hypertrophy.