TRP channels as mediators of oxidative stress

Barbara Miller, Wenyi Zhang

Research output: Chapter in Book/Report/Conference proceedingConference contribution

66 Citations (Scopus)

Abstract

The transient receptor potential (TRP) protein superfamily is a diverse group of cation-permeable channels expressed in mammalian cells, which is divided into six subfamilies based on sequence identity. Three subfamilies have members with roles in oxidative stress: the TRPC subfamily characterized by receptor operated calcium entry channels; the TRPM subfamily with a number of members involved in cell proliferation and death; and the TRPV subfamily which is activated by chemical, mechanical, and physical stimuli. The TRPC members TRPC3 and TRPC4 can serve as subunits of a redox-sensitive ion channel in native aortic endothelial cells. The TRPM family member TRPM2 has a number of physiologic isoforms expressed in many cell types and responds to stimuli including oxidative stress, TNFα, and β-amyloid peptide. The important role of TRPM2 isoforms in cell proliferation and oxidant-induced cell death has been well established using divergent cell systems and techniques including overexpression, channel depletion or inhibition, and calcium chelation. TRPM7 has been shown to be involved in Ca 2+ influx and anoxic cell death in cortical neurons. In these cells and in B cells, precise expression of TRPM7 is necessary for cell survival. TRPV1 is involved in oxidant stress-induced pain and in neuronal injury, contributing to diabetic sensory neuropathy. Future studies will likely identify additional channels involved in oxidant injury, as well as better define mechanisms through which these channels are regulated and mediate their effects. Therapeutic approaches to modulate activation of specific TRP channels are likely to have an important impact in reducing tissue damage in a number of diseases resulting from oxidant stress including ischemia/reperfusion injury and diabetes.

Original languageEnglish (US)
Title of host publicationTransient Receptor Potential Channels
EditorsShahidul Islam, Shahidul Islam
Pages531-544
Number of pages14
DOIs
StatePublished - Dec 15 2011

Publication series

NameAdvances in Experimental Medicine and Biology
Volume704
ISSN (Print)0065-2598

Fingerprint

Transient Receptor Potential Channels
Oxidative stress
Oxidants
Oxidative Stress
Cell death
Cell Death
Cells
Cell proliferation
Protein Isoforms
Cell Proliferation
Calcium-Sensing Receptors
Diabetic Neuropathies
Endothelial cells
Wounds and Injuries
Calcium Channels
Medical problems
Chelation
Reperfusion Injury
Ion Channels
Amyloid

All Science Journal Classification (ASJC) codes

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Miller, B., & Zhang, W. (2011). TRP channels as mediators of oxidative stress. In S. Islam, & S. Islam (Eds.), Transient Receptor Potential Channels (pp. 531-544). (Advances in Experimental Medicine and Biology; Vol. 704). https://doi.org/10.1007/978-94-007-0265-3_29
Miller, Barbara ; Zhang, Wenyi. / TRP channels as mediators of oxidative stress. Transient Receptor Potential Channels. editor / Shahidul Islam ; Shahidul Islam. 2011. pp. 531-544 (Advances in Experimental Medicine and Biology).
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Miller, B & Zhang, W 2011, TRP channels as mediators of oxidative stress. in S Islam & S Islam (eds), Transient Receptor Potential Channels. Advances in Experimental Medicine and Biology, vol. 704, pp. 531-544. https://doi.org/10.1007/978-94-007-0265-3_29

TRP channels as mediators of oxidative stress. / Miller, Barbara; Zhang, Wenyi.

Transient Receptor Potential Channels. ed. / Shahidul Islam; Shahidul Islam. 2011. p. 531-544 (Advances in Experimental Medicine and Biology; Vol. 704).

Research output: Chapter in Book/Report/Conference proceedingConference contribution

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AB - The transient receptor potential (TRP) protein superfamily is a diverse group of cation-permeable channels expressed in mammalian cells, which is divided into six subfamilies based on sequence identity. Three subfamilies have members with roles in oxidative stress: the TRPC subfamily characterized by receptor operated calcium entry channels; the TRPM subfamily with a number of members involved in cell proliferation and death; and the TRPV subfamily which is activated by chemical, mechanical, and physical stimuli. The TRPC members TRPC3 and TRPC4 can serve as subunits of a redox-sensitive ion channel in native aortic endothelial cells. The TRPM family member TRPM2 has a number of physiologic isoforms expressed in many cell types and responds to stimuli including oxidative stress, TNFα, and β-amyloid peptide. The important role of TRPM2 isoforms in cell proliferation and oxidant-induced cell death has been well established using divergent cell systems and techniques including overexpression, channel depletion or inhibition, and calcium chelation. TRPM7 has been shown to be involved in Ca 2+ influx and anoxic cell death in cortical neurons. In these cells and in B cells, precise expression of TRPM7 is necessary for cell survival. TRPV1 is involved in oxidant stress-induced pain and in neuronal injury, contributing to diabetic sensory neuropathy. Future studies will likely identify additional channels involved in oxidant injury, as well as better define mechanisms through which these channels are regulated and mediate their effects. Therapeutic approaches to modulate activation of specific TRP channels are likely to have an important impact in reducing tissue damage in a number of diseases resulting from oxidant stress including ischemia/reperfusion injury and diabetes.

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Miller B, Zhang W. TRP channels as mediators of oxidative stress. In Islam S, Islam S, editors, Transient Receptor Potential Channels. 2011. p. 531-544. (Advances in Experimental Medicine and Biology). https://doi.org/10.1007/978-94-007-0265-3_29