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Nitric oxide lacks direct effect on TRPC5 channels but suppresses endogenous TRPC5-containing channels in endothelial

Ching-On Wong1, Piruthivi Sukumar, David J Beech

  • 1Li Ka Shing Insitute of Health Sciences and School of Biomedical Sciences, The Chinese University of Hong Kong, Shatin, Hong Kong, People's Republic of China.

Pflugers Archiv : European Journal of Physiology
|April 15, 2010
PubMed

Insights

Nitric oxide does not directly modulate TRPC5 channels. However, it may inhibit endothelial cell channels containing TRPC5, suggesting a role in regulating calcium signaling in these cells.

Area of Science:

  • Molecular biology
  • Cell physiology
  • Ion channel function

Background:

  • Transient receptor potential canonical 5 (TRPC5) forms cation channels in various cells, including neurons and endothelial cells.
  • TRPC5 channels are activated by diverse stimuli, but their sensitivity to nitric oxide (NO) remains unclear.

Purpose of the Study:

  • To investigate the direct effect of nitric oxide on TRPC5 channel activity.
  • To determine if TRPC5 channels are modulated by nitric oxide in native endothelial cells.

Main Methods:

  • Overexpression of mouse and human TRPC5 in HEK293 cells.
  • Measurement of intracellular calcium concentration and membrane currents to assess TRPC5 activity.
  • Application of nitric oxide donors (SNAP, DEA-NONOate) and TRPC5-specific antibodies/mutants in HEK293 cells and bovine aortic endothelial cells (BAECs).

Main Results:

  • Nitric oxide donors (SNAP, DEA-NONOate) did not directly stimulate or inhibit heterologously expressed TRPC5 channels.
  • High concentrations of SNAP showed inconsistent TRPC5 activation, confounded by non-specific calcium signals.
  • Nitric oxide donor SNAP suppressed endogenous calcium entry in BAECs, an effect dependent on TRPC5.

Conclusions:

  • Nitric oxide does not directly modulate homomeric TRPC5 channels.
  • Nitric oxide may inhibit endogenous endothelial cell channels containing TRPC5, impacting calcium influx.

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