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Related Experiment Videos

Mechanical stretch induces podocyte hypertrophy in vitro.

Arndt T Petermann1, Jeffrey Pippin, Raghu Durvasula

  • 1Department of Medicine, Division of Nephrology, University of Washington School of Medicine, Seattle, Washington 98195, USA.

Kidney International
|December 22, 2004
PubMed
Summary

Mechanical stretch causes podocyte hypertrophy, a process dependent on cell cycle entry, p21, Erk1/2, and Akt. This finding is crucial for understanding podocyte injury in conditions with increased intraglomerular pressure.

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Area of Science:

  • Nephrology
  • Cell Biology
  • Mechanobiology

Background:

  • Increased intraglomerular pressure contributes to glomerulosclerosis in various kidney diseases.
  • Mechanical stretch (stress-tension) on glomerular cells is a consequence of elevated intraglomerular pressure.
  • The impact of mechanical stretch on podocyte growth and its underlying mechanisms remain unclear.

Purpose of the Study:

  • To investigate the effects of mechanical stretch on podocyte growth.
  • To elucidate the molecular mechanisms involved in stretch-induced podocyte alterations.
  • To determine the role of cell cycle regulators and signaling pathways in podocyte response to stretch.

Main Methods:

  • Cultured mouse podocytes were subjected to cyclic mechanical stretch.

Related Experiment Videos

  • Cell proliferation and hypertrophy were assessed using flow cytometry.
  • The involvement of cyclin-dependent kinase inhibitors (p21, p27) and signaling pathways (Erk1/2, Akt, p38) was evaluated in knockout models and via blocking studies.

    • Main Results:

    • Mechanical stretch induced podocyte hypertrophy across all cell cycle phases in wild-type and p27 knockout cells.
    • Hypertrophy was dependent on cell cycle entry and the presence of p21.
    • Blocking Erk1/2 or Akt pathways prevented stretch-induced hypertrophy, while p38 activation did not influence this outcome.

    Conclusions:

    • Mechanical stretch in vitro induces podocyte hypertrophy in a cell cycle-dependent manner.
    • This process requires p21, Erk1/2, and Akt signaling.
    • Mechanical stretch may contribute to podocyte injury under conditions of elevated intraglomerular pressure.