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Shear-induced volume decrease in MDCK cells.

Jinseok Heo1, Frederick Sachs, Jianbin Wang

  • 1Department of Physiology and Biophysics, SUNY-Buffalo, Buffalo, NY 14260, USA.

Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology
|July 5, 2012
PubMed
Summary
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Shear stress causes Madin-Darby Canine Kidney (MDCK) cells to irreversibly shrink by 20-30%. This cell shrinkage is mediated by aquaporins and not by common ion channels, suggesting a pressure-driven water efflux mechanism.

Area of Science:

  • Cell Biology
  • Biophysics
  • Fluid Mechanics

Background:

  • Cell volume regulation is crucial for cellular function.
  • Shear stress is a significant physical force cells encounter in physiological environments.
  • Understanding cell volume changes under mechanical stress is vital for various biological processes.

Purpose of the Study:

  • To investigate the effect of shear stress on Madin-Darby Canine Kidney (MDCK) cell volume.
  • To elucidate the mechanisms underlying shear-induced cell volume changes.
  • To determine the reversibility and ionic dependencies of shear-induced cell shrinkage.

Main Methods:

  • Microfluidic cell volume sensing to measure real-time cell volume changes.
  • Fluorescence quenching assays to confirm volume reduction.

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  • Pharmacological inhibition using Hg(2+), TEA, DIDS, and Gd(3+) to probe ion channel involvement.
  • Finite element mechanical modeling to simulate intracellular pressure.
  • Main Results:

    • Increased shear stress (0.2 to 2.0 dyn/cm(2)) induced a 20-30% irreversible cell volume decrease in MDCK cells.
    • Cell shrinkage was significantly inhibited by Hg(2+), implicating aquaporins in water efflux.
    • Volume reduction was independent of K(+) and Cl(-) channels, cationic stretch-activated ion channels (SACs), and intracellular Ca(2+).

    Conclusions:

    • Shear stress induces irreversible cell shrinkage in MDCK cells, likely via aquaporin-mediated water efflux.
    • The mechanism appears to be driven by increased intracellular hydrostatic pressure due to cell deformation under flow.
    • This process is distinct from typical regulatory volume decrease (RVD) mechanisms.