Linked Life Data

17499219

Source:http://linkedlifedata.com/resource/pubmed/id/17499219

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2007-5-29
pubmed:abstractText
Non-steroidal anti-inflammatory drugs (NSAIDs) contribute to gastrointestinal ulcer formation by inhibiting epithelial cell migration and mucosal restitution; however, the drug-affected signaling pathways are poorly defined. We investigated whether NSAID inhibition of intestinal epithelial migration is associated with depletion of intracellular polyamines, depolarization of membrane potential (E(m)) and altered surface expression of K(+) channels. Epithelial cell migration in response to the wounding of confluent IEC-6 and IEC-Cdx2 monolayers was reduced by indomethacin (100 microM), phenylbutazone (100 microM) and NS-398 (100 microM) but not by SC-560 (1 microM). NSAID-inhibition of intestinal cell migration was not associated with depletion of intracellular polyamines. Treatment of IEC-6 and IEC-Cdx2 cells with indomethacin, phenylbutazone and NS-398 induced significant depolarization of E(m), whereas treatment with SC-560 had no effect on E(m). The E(m) of IEC-Cdx2 cells was: -38.5+/-1.8 mV under control conditions; -35.9+/-1.6 mV after treatment with SC-560; -18.8+/-1.2 mV after treatment with indomethacin; and -23.7+/-1.4 mV after treatment with NS-398. Whereas SC-560 had no significant effects on the total cellular expression of K(v)1.4 channel protein, indomethacin and NS-398 decreased not only the total cellular expression of K(v)1.4, but also the cell surface expression of both K(v)1.4 and K(v)1.6 channel subunits in IEC-Cdx2. Both K(v)1.4 and K(v)1.6 channel proteins were immunoprecipitated by K(v)1.4 antibody from IEC-Cdx2 lysates, indicating that these subunits co-assemble to form heteromeric K(v) channels. These results suggest that NSAID inhibition of epithelial cell migration is independent of polyamine-depletion, and is associated with depolarization of E(m) and decreased surface expression of heteromeric K(v)1 channels.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0006-2952
pubmed:author
pubmed:issnType
Print
pubmed:day
30
pubmed:volume
74
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
74-85
pubmed:dateRevised
2007-12-3
pubmed:meshHeading
pubmed-meshheading:17499219-Anti-Inflammatory Agents, Non-Steroidal, pubmed-meshheading:17499219-Cell Line, pubmed-meshheading:17499219-Cell Membrane, pubmed-meshheading:17499219-Cell Movement, pubmed-meshheading:17499219-Chromatography, High Pressure Liquid, pubmed-meshheading:17499219-Humans, pubmed-meshheading:17499219-Indomethacin, pubmed-meshheading:17499219-Intestinal Mucosa, pubmed-meshheading:17499219-Membrane Potentials, pubmed-meshheading:17499219-Nitrobenzenes, pubmed-meshheading:17499219-Patch-Clamp Techniques, pubmed-meshheading:17499219-Phenylbutazone, pubmed-meshheading:17499219-Polyamines, pubmed-meshheading:17499219-Shaker Superfamily of Potassium Channels, pubmed-meshheading:17499219-Signal Transduction, pubmed-meshheading:17499219-Spectrometry, Mass, Electrospray Ionization, pubmed-meshheading:17499219-Sulfonamides, pubmed-meshheading:17499219-Wound Healing
pubmed:year
2007
pubmed:articleTitle
Depolarization and decreased surface expression of K+ channels contribute to NSAID-inhibition of intestinal restitution.
pubmed:affiliation
Department of Anatomy and Physiology, Kansas State University, Manhattan, KS 66506, United States.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural