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Hypotonicity-induced TRPV4 function in renal collecting duct cells: modulation by progressive cross-talk with

Min Jin1, Jonathan Berrout, Ling Chen

  • 1Dept. of Integrative Biology and Pharmacology, The University of Texas Health Science Center, Houston, TX 77030, USA.

Cell Calcium
|December 30, 2011
PubMed

Insights

TRPV4 channels interact with SK3 and BK-α channels in mouse kidney cells. This cross-talk regulates calcium (Ca2+) influx and potassium (K+) channel activity, suggesting a progressive activation mechanism.

Area of Science:

  • Physiology
  • Molecular Biology
  • Renal Cell Biology

Background:

  • The cortical collecting duct (CCD) plays a crucial role in kidney function.
  • TRPV4 channels are involved in cellular responses to osmotic stress.
  • Calcium-activated potassium channels (SK3 and BKα) are critical for regulating cell membrane potential.

Purpose of the Study:

  • To investigate the functional interaction between TRPV4 and Ca(2+)-activated K(+) channels (SK3 and BKα) in mouse CCD M-1 cells.
  • To elucidate the role of TRPV4 in regulating the activity of SK3 and BKα channels.
  • To understand the reciprocal regulation of TRPV4 activity by SK3 and BKα channels.

Main Methods:

  • Immunocytochemistry to detect protein expression of TRPV4, aquaporin-2, SK3, and BKα channels.
  • TRPV4 overexpression studies.
  • Pharmacological activation and inhibition of TRPV4 using agonist GSK1016790A and antagonist HC-067047.
  • Selective inhibition of SK3 and BKα channels using apamin and Iberiotoxin, respectively.

Main Results:

  • TRPV4, aquaporin-2, SK3, and BKα channels are co-expressed in mouse CCD M-1 cells.
  • TRPV4 activation by hypotonic swelling or agonist leads to increased SK3 and BKα channel activity, dependent on TRPV4-mediated Ca(2+) influx.
  • Inhibition of SK3 or BKα channels enhances TRPV4-mediated Ca(2+) influx, indicating a reciprocal dependency.

Conclusions:

  • A synergistic cross-talk exists between TRPV4, SK3, and BKα channels in mouse CCD cells.
  • This interaction provides tight functional regulation between these channel groups.
  • The cross-talk may involve a progressive activation: TRPV4-mediated Ca(2+) influx activates SK3, which then enhances Ca(2+) influx to activate BKα.

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