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Receptor Tyrosine and MAP Kinase are Involved in Effects of H(2)O(2) on Interstitial Cells of Cajal in Murine Intestine

Cited 8 time in Web of Science Cited 8 time in Scopus
Authors
Choi, Seok; Yeum, Cheol Ho; Kim, Young Dae; Park, Chan Guk; Kim, Man Yoo; Park, Jong-Seong; Jeong, Han-Seong; Kim, Byung Joo; So, Insuk; Kim, Ki Whan; Jun, Jae Yeoul
Issue Date
2008-07-16
Publisher
Wiley-Blackwell
Citation
J Cell Mol Med. 2008; 141: 257-266
Keywords
Hydrogen peroxideInterstitial cells of CajalPacemaker currentsCyclooxygenaseReceptor tyrosine kinaseMAP kinase
Abstract
Hydrogen peroxide (H(2)O(2)) is involved in intestinal motility through changes of smooth muscle activity. However, there is no report as to the modulatory effects of H(2)O(2) on interstitial cells of Cajal (ICC). We investigated the H(2)O(2) effects and signal transductions to determine whether the intestinal motility can be modulated through ICC. We performed whole-cell patch clamp in cultured ICC from murine intestine and molecular analyses. H(2)O(2) hyperpolarized the membrane and inhibited pacemaker currents. These effects were inhibited by glibenclamide, an inhibitor of ATP-sensitive K(+) (K(ATP)) channels. The free radical scavenger catalase inhibited the H(2)O(2)-induced effects. MAFP and AACOCF(3) (a cytosolic phospholipase A(2) inhibitors) or SC-560 and NS-398 (a selective COX-1 and 2 inhibitor) or AH6809 (an EP(2) receptor antagonist) inhibited the H(2)O(2)-induced effects. PD98059 (a mitogen activated/ERK-activating protein kinase inhibitor) inhibited the H(2)O(2)-induced effects, though SB-203580 (a p38 MAPK inhibitor) or a JNK inhibitor did not affect. H(2)O(2)-induced effects could not be inhibited by LY-294002 (an inhibitor of PI(3)-kinases), calphostin C (a protein kinase C inhibitor), or SQ-22536 (an adenylate cyclase inhibitor). Adenoviral infection analysis revealed H(2)O(2) stimulated tyrosine kinase activity and AG 1478 (an antagonist of epidermal growth factor receptor tyrosine kinase) inhibited the H(2)O(2)-induced effects. These results suggest H(2)O(2) can modulate ICC pacemaker activity and this occur by the activation of K(ATP) channels through PGE(2) production via receptor tyrosine kinase-dependent MAP kinase activation.
Language
English
URI
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=18624754

http://hdl.handle.net/10371/68490
DOI
https://doi.org/10.1111/j.1582-4934.2008.00403.x

https://doi.org/10.1111/j.1582-4934.2008.00403.x
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College of Medicine/School of Medicine (의과대학/대학원)Dept. of Physiology (생리학교실)Journal Papers (저널논문_생리학교실)
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