Inhibition of pacemaker activity in interstitial cells of Cajal by LPS via NF-κB and MAP kinase

To investigate lipopolysaccharide (LPS) related signal transduction in interstitial cells of Cajal (ICCs) from mouse small intestine. For this study, primary culture of ICCs was prepared from the small intestine of the mouse. LPS was treated to the cells prior to measurement of the membrane currents...

Full description

Saved in:
Bibliographic Details
Published in:World journal of gastroenterology : WJG 2013-02, Vol.19 (8), p.1210-1218
Main Authors: Zuo, Dong Chuan, Choi, Seok, Shahi, Pawan Kumar, Kim, Man Yoo, Park, Chan Guk, Kim, Young Dae, Lee, Jun, Chang, In Yeoup, So, Insuk, Jun, Jae Yeoul
Format: Article
Language:English
Subjects:
Animals
Antioxidants - pharmacology
Biological Clocks - drug effects
Cells, Cultured
Cyclooxygenase 2 - metabolism
Cyclooxygenase 2 Inhibitors - pharmacology
Dinoprostone - metabolism
Female
Interstitial Cells of Cajal - drug effects
Interstitial Cells of Cajal - enzymology
Intestine, Small - cytology
Intestine, Small - drug effects
Intestine, Small - enzymology
Lipopolysaccharides - pharmacology
Male
MAP Kinase Signaling System - drug effects
Membrane Potentials
Mice
Mice, Inbred BALB C
NF-kappa B - metabolism
Nitric Oxide - metabolism
Nitric Oxide Synthase Type II - antagonists & inhibitors
Nitric Oxide Synthase Type II - metabolism
Original
Periodicity
Primary Cell Culture
Protein Kinase Inhibitors - pharmacology
Toll-Like Receptor 4 - drug effects
Toll-Like Receptor 4 - metabolism
Citations: Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:To investigate lipopolysaccharide (LPS) related signal transduction in interstitial cells of Cajal (ICCs) from mouse small intestine. For this study, primary culture of ICCs was prepared from the small intestine of the mouse. LPS was treated to the cells prior to measurement of the membrane currents by using whole-cell patch clamp technique. Immunocytochemistry was used to examine the expression of the proteins in ICCs. LPS suppressed the pacemaker currents of ICCs and this could be blocked by AH6809, a prostaglandin E2-EP2 receptor antagonist or NG-Nitro-L-arginine Methyl Ester, an inhibitor of nitric oxide (NO) synthase. Toll-like receptor 4, inducible NO synthase or cyclooxygenase-2 immunoreactivity by specific antibodies was detected on ICCs. Catalase (antioxidant agent) had no action on LPS-induced action in ICCs. LPS actions were blocked by nuclear factor κB (NF-κB) inhibitor, actinomycin D (a gene transcription inhibitor), PD 98059 (a p42/44 mitogen-activated protein kinases inhibitor) or SB 203580 [a p38 mitogen-activated protein kinases (MAPK) inhibitor]. SB 203580 also blocked the prostaglandin E2-induced action on pacemaker currents in ICCs but not NO. LPS inhibit the pacemaker currents in ICCs via prostaglandin E2- and NO-dependent mechanism through toll-like receptor 4 and suggest that MAPK and NF-κB are implicated in these actions.
ISSN:1007-9327
2219-2840
DOI:10.3748/wjg.v19.i8.1210