Role of reactive oxygen species and redox in regulating the function of transient receptor potential channels

Michael Y. Song, Ayako Makino, Jason X.J. Yuan

Research output: Contribution to journalReview article

31 Scopus citations

Abstract

Cellular redox status, regulated by production of reactive oxygen species (ROS), greatly contributes to the regulation of vascular smooth muscle cell contraction, migration, proliferation, and apoptosis by modulating the function of transient receptor potential (TRP) channels in the plasma membrane. ROS functionally interact with the channel protein via oxidizing the redox-sensitive residues, whereas nitric oxide (NO) regulates TRP channel function by cyclic GMP/protein kinase G-dependent and-independent pathways. Based on the structural differences among different TRP isoforms, the effects of ROS and NO are also different. In addition to regulating TRP channels in the plasma membrane, ROS and NO also modulate Ca 2+ release channels (e.g., IP 3 and ryanodine receptors) on the sarcoplasmic/endoplasmic reticulum membrane. This review aims at briefly describing (a) the role of TRP channels in receptor-operated and store-operated Ca 2+ entry, and (b) the role of ROS and redox status in regulating the function and structure of TRP channels.

Original languageEnglish (US)
Pages (from-to)1549-1565
Number of pages17
JournalAntioxidants and Redox Signaling
Volume15
Issue number6
DOIs
StatePublished - Sep 15 2011
Externally publishedYes

ASJC Scopus subject areas

  • Biochemistry
  • Physiology
  • Molecular Biology
  • Clinical Biochemistry
  • Cell Biology

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