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Bladder Smooth Muscle Strip Contractility as a Method to Evaluate Lower Urinary Tract Pharmacology
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Effect of sustained hydrostatic pressure on rat bladder smooth muscle cell function.

Margaret Rebecca Drumm1, Brittany D York, Jiro Nagatomi

  • 1Department of Bioengineering, Rhodes Engineering Research Center, Clemson University, Clemson, South Carolina 29634-0905, USA.

Urology
|October 30, 2009
PubMed
Summary

Elevated hydrostatic pressure causes bladder smooth muscle cells (BSMCs) to change shape and proliferate, potentially indicating a shift from contractile to synthetic phenotypes. The ERK(1/2) pathway may drive this pressure-induced cell growth.

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Area of Science:

  • Urology
  • Cell Biology
  • Biomedical Engineering

Background:

  • Mechanical stimuli are crucial for bladder development, but the precise mechanisms are not fully understood.
  • Bladder smooth muscle cells (BSMCs) are key components of bladder function and development.
  • Understanding cellular responses to mechanical stress is vital for regenerative medicine and disease treatment.

Purpose of the Study:

  • To investigate whether elevated hydrostatic pressure induces a phenotypic shift in BSMCs from contractile to synthetic.
  • To explore the role of the extracellular signal-regulated kinase (ERK(1/2)) pathway in pressure-induced BSMC changes.

Main Methods:

  • Rat BSMCs were subjected to 7.5 cm H2O hydrostatic pressure for up to 48 hours.
  • Cell morphology and proliferation were quantified using imaging techniques.

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  • Western blotting assessed ERK(1/2) activation and expression of contractile proteins (alpha-smooth muscle actin, SM-22).

    • Main Results:

    • Hydrostatic pressure led to a more spread BSMC morphology within 4 hours.
    • Activated ERK(1/2) expression peaked at 1.5-3 hours, showing up to a two-fold increase.
    • BSMC density increased after 48 hours of pressure exposure, while contractile protein levels remained unchanged.

    Conclusions:

    • Morphological and proliferative changes suggest a pressure-induced shift in BSMC phenotype from contractile to synthetic.
    • ERK(1/2) pathway activation appears to be a potential mechanism for pressure-induced BSMC proliferation.
    • The study indicates that not all BSMC phenotype markers are regulated simultaneously by hydrostatic pressure.