PMID- 15104185
OWN - NLM
STAT- MEDLINE
DCOM- 20040513
LR  - 20131121
IS  - 1528-2511 (Print)
IS  - 1528-2511 (Linking)
VI  - 258
DP  - 2004
TI  - Role of TRP channels in oxidative stress.
PG  - 222-30; discussion 231-5, 263-6
AB  - Increasing evidence suggests a pivotal role of reactive oxygen species (ROS) as 
      well as reactive nitrogen species (RNS) in human pathophysiology. A typical 
      target of ROS/RNS signalling is Ca2+ channels which mediate both long-term as 
      well as acute cellular responses to oxidative stress. We have previously reported 
      that cation channels related to the Drosophila transient receptor potential gene 
      product (TRPC proteins) are likely to serve as redox sensors in the vascular 
      endothelium, and demonstrated that TRPC3 expression is a determinant of the 
      nitric oxide sensitivity of store-operated Ca2+ signalling. Experiments with TRPC 
      species overexpressed in HEK293 cells confirmed that TRPC3 and TRPC4 are able to 
      form redox sensitive cation channels. A key mechanism involved in redox 
      activation of TRPC3 appears to be ROS-induced promotion of protein tyrosine 
      phosphorylation and stimulation of phospholipase C activity. In addition, 
      oxidative stress-induced disruption of caveolin 1-rich lipid raft domains, which 
      interfere with functional TRPC channels, is likely to contribute to redox 
      modulation of TRP proteins and to oxidative stress-induced changes in cellular 
      Ca2+ signalling. Taken together, our data suggest TRPC species serve as a link 
      between cellular redox state and Ca2+ homeostasis. Thus, modulation of these 
      cellular redox sensors may offer unique opportunities for therapeutic 
      interventions.
FAU - Groschner, Klaus
AU  - Groschner K
AD  - Department of Pharmacology and Toxicology, Karl-Franzens-University, University 
      of Graz, Universitaetsplatz 2, A -8010 Graz, Austria.
FAU - Rosker, Christian
AU  - Rosker C
FAU - Lukas, Michael
AU  - Lukas M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Novartis Found Symp
JT  - Novartis Foundation symposium
JID - 9807767
RN  - 0 (CAV1 protein, human)
RN  - 0 (Caveolin 1)
RN  - 0 (Caveolins)
RN  - 0 (Ion Channels)
RN  - 0 (Peroxides)
RN  - 0 (TRPC Cation Channels)
RN  - 0 (TRPC3 cation channel)
RN  - 97C5T2UQ7J (Cholesterol)
RN  - 9NEZ333N27 (Sodium)
RN  - EC 3.1.4.- (Type C Phospholipases)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Calcium/*physiology
MH  - Calcium Signaling/*physiology
MH  - Caveolin 1
MH  - Caveolins/metabolism
MH  - Cells, Cultured
MH  - Cholesterol/metabolism
MH  - Endothelial Cells/metabolism
MH  - Humans
MH  - Ion Channels/chemistry/genetics/*metabolism
MH  - Oxidation-Reduction
MH  - *Oxidative Stress
MH  - Peroxides/pharmacology
MH  - Sodium/metabolism
MH  - TRPC Cation Channels
MH  - Type C Phospholipases/pharmacology
EDAT- 2004/04/24 05:00
MHDA- 2004/05/14 05:00
CRDT- 2004/04/24 05:00
PHST- 2004/04/24 05:00 [pubmed]
PHST- 2004/05/14 05:00 [medline]
PHST- 2004/04/24 05:00 [entrez]
PST - ppublish
SO  - Novartis Found Symp. 2004;258:222-30; discussion 231-5, 263-6.