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Stretch activates heparin-binding EGF-like growth factor expression in bladder smooth muscle cells
J M Park1, J G Borer, M R Freeman
1Urologic Laboratory, Department of Urology, Children's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA.
The American Journal of Physiology
|November 14, 1998
Summary
Mechanical stretch increases heparin-binding epidermal growth factor (HB-EGF) gene expression in rat bladder smooth muscle cells. This process is partly mediated by autocrine angiotensin II (ANG II) secretion, influencing cell growth.
Area of Science:
- Cell Biology
- Physiology
- Biochemistry
Background:
- Bladder smooth muscle cells (SMC) are crucial for bladder function.
- Mechanical forces, such as stretch, can influence cellular behavior and gene expression in SMC.
Purpose of the Study:
- To investigate the effect of mechanical stretch on heparin-binding epidermal growth factor (HB-EGF) expression in rat bladder SMC.
- To elucidate the role of autocrine angiotensin II (ANG II) in mediating stretch-induced HB-EGF expression.
Main Methods:
- Cultured rat bladder SMC were subjected to mechanical stretch-relaxation cycles.
- RT-PCR and immunostaining were used to analyze HB-EGF mRNA and protein levels.
- Reporter gene assays and thymidine incorporation measured gene activation and cell proliferation.
Main Results:
- Mechanical stretch significantly increased HB-EGF mRNA and protein expression in bladder SMC.
- Stretch led to increased autocrine ANG II secretion and activation of the ANG II receptor type 1.
- Losartan, an ANG II receptor antagonist, suppressed stretch-induced HB-EGF expression and thymidine incorporation.
Conclusions:
- Mechanical stretch activates HB-EGF gene expression in bladder SMC.
- Autocrine ANG II signaling plays a partial role in mediating the response to mechanical stretch.
- These findings suggest a mechanism linking mechanical stimuli to SMC growth and function.