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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, Jong-Seong; Jeong, Han-Seong; Kim, Man Yoo; Park, Chan Guk; Kim, Byung Joo; Kim, Ki Whan; Jun, Jae Yeoul; So, Insuk
Issue Date
2010-02
Publisher
WILEY-BLACKWELL PUBLISHING, INC
Citation
JOURNAL OF CELLULAR AND MOLECULAR MEDICINE; Vol.14, No 1-2; 257-266
Keywords
hydrogen peroxidepacemaker currentscyclooxygenaseMAP kinasereceptor tyrosine kinaseinterstitial cells of Cajal
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.
ISSN
1582-1838
Language
English
URI
https://hdl.handle.net/10371/76239
DOI
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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