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Modulation of staurosporine-activated volume-sensitive outwardly rectifying Cl⁻ channel by PI3K/Akt in cardiomyocytes

Yan Liu1, Bo Wang, Wei-Wei Zhang

  • 1Department of Geriatrics, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China.

Current Pharmaceutical Design
|January 18, 2013
PubMed

Insights

Staurosporine (STS) activates volume-sensitive outwardly rectifying chloride (Cl⁻) channels (I(Cl,Vol)) in cardiomyocytes, potentially through a phosphatidylinositol-3 kinase (PI3K)/Akt pathway, offering new insights into cardiac stress responses.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Ion Channel Physiology

Background:

  • Chloride (Cl⁻) channels regulate cardiac function during stress.
  • The precise regulatory mechanisms of cardiac Cl⁻ channels remain unclear.
  • Volume-sensitive outwardly rectifying Cl⁻ current (I(Cl,Vol)) plays a role in cellular function.

Purpose of the Study:

  • To investigate the effect of staurosporine (STS), a pro-apoptotic stimulus, on I(Cl,Vol) in cardiomyocytes.
  • To explore the potential involvement of the phosphatidylinositol-3 kinase (PI3K)/Akt signaling pathway in STS-induced I(Cl,Vol) activation.

Main Methods:

  • Primary cultured rat neonatal cardiomyocytes were used.
  • Cells were exposed to hypotonic and isotonic conditions with or without STS.
  • Whole-cell voltage-clamp technique was employed to measure Cl⁻ currents.

Main Results:

  • STS activated an outwardly rectifying Cl⁻ current in cardiomyocytes, resembling I(Cl,Vol).
  • This current was inhibited by DIDS and DCPIB, confirming its identity as I(Cl,Vol).
  • PI3K inhibitor LY294002 facilitated the current, while insulin partially inhibited it, suggesting PI3K/Akt pathway involvement.

Conclusions:

  • Staurosporine activates I(Cl,Vol) channels in cardiomyocytes.
  • This activation appears to be mediated, at least in part, by a PI3K/Akt-dependent mechanism.
  • Findings provide new understanding of cardiac Cl⁻ channel regulation under stress.

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