Abstract:
BACKGROUND AND PURPOSE:Lipopolysaccharide (LPS) induces intestinal dysmotility by alteration of smooth muscle and enteric neuronal activities. However, there is no report on the modulatory effects of LPS on the interstitial cells of Cajal (ICCs). We investigated the effect of LPS and its signal transduction in ICCs. METHODS:We performed whole-cell patch clamp and RT-PCR in cultured ICCs from mouse small intestine. RESULTS:LPS suppressed the generation of pacemaker currents of ICCs. The mRNA transcripts for Toll-like receptor 4 (TLR4) were expressed in ICCs. However, the inhibitory action of LPS on pacemaker currents from TLR4(+/+) mice was not present in TLR4(-/-) mice. The inhibitory effects of LPS on ICCs were blocked by glibenclamide (an inhibitor of ATP-sensitive K(+) channels), NS-398 (a COX-2 inhibitor), AH6808 [a prostaglandin E(2) (PGE(2))-EP(2) receptor antagonist], ODQ (an inhibitor of guanylate cyclase) and L-NAME [an inhibitor of nitric oxide synthase (NOS)]. Furthermore, genistein and herbimycin A (tyrosine kinase inhibitors) blocked the LPS-induced inhibitory action on pacemaker activity in ICCs. CONCLUSIONS:LPS can activate ICCs to release NO and PGE(2) through TLR4 activation. The released NO and PGE(2) inhibit pacemaker currents by activating ATP-sensitive K(+) channels. The LPS actions are mediated by tyrosine kinase signaling pathways.
journal_name
Pharmacologyjournal_title
Pharmacologyauthors
Zuo DC,Choi S,Shahi PK,Kim MY,Park CG,Kim YD,Lee J,Chang IY,Lee HS,Yeom SC,Moon HJ,Seong SY,So I,Jun JYdoi
10.1159/000340018subject
Has Abstractpub_date
2012-01-01 00:00:00pages
151-9issue
3-4eissn
0031-7012issn
1423-0313pii
000340018journal_volume
90pub_type
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