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Article: Involvement of voltage-gated K+ and Na+ channels in gastric epithelial cell migration

TitleInvolvement of voltage-gated K+ and Na+ channels in gastric epithelial cell migration
Authors
Issue Date2008
PublisherSpringer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0300-8177
Citation
Molecular And Cellular Biochemistry, 2008, v. 308 n. 1-2, p. 219-226 How to Cite?
AbstractEpithelial cell migration plays an important role in gastrointestinal mucosal repair. We previously reported that multiple functional ion channels, including a Ba2+-sensitive K+ inward rectifier Kir1.2, 4-aminopyridine (4-AP)-sensitive voltage-gated K+ channels Kv1.1, Kv1.6 and Kv2.1, and a nifedipine-sensitive, tetrodotoxin (TTX)-insensitive voltage-gated Na+ channel Nav1.5 were expressed in a non-transformed rat gastric epithelial cell line (RGM-1). In the present study, we further investigated whether these ion channels are involved in the modulation of gastric epithelial cell migration. Cell migration was determined by monolayer wound healing assay. Results showed that blockade of Kv with 4-AP or Nav1.5 with nifedipine inhibited RGM-1 cell migration in the absence or presence of epidermal growth factor (EGF), which effectively stimulated RGM-1 cell migration. Moreover, high concentration of TTX mimicked the action of nifedipine, suggesting that the action of nifedipine was mediated through specific blockade of Nav1.5. In contrast, inhibition of Kir1.2 with Ba2+, either in basal or EGF-stimulated condition, had no effect on RGM-1 cell migration. In conclusion, the present study demonstrates for the first time that voltage-gated K+ and Na+ channels are involved in the modulation of gastric epithelial cell migration. © Springer Science+Business Media, LLC. 2007.
Persistent Identifierhttp://hdl.handle.net/10722/163139
ISSN
2015 Impact Factor: 2.613
2015 SCImago Journal Rankings: 1.019
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWu, WKKen_US
dc.contributor.authorLi, GRen_US
dc.contributor.authorWong, TMen_US
dc.contributor.authorWang, JYen_US
dc.contributor.authorYu, Len_US
dc.contributor.authorCho, CHen_US
dc.date.accessioned2012-09-05T05:28:04Z-
dc.date.available2012-09-05T05:28:04Z-
dc.date.issued2008en_US
dc.identifier.citationMolecular And Cellular Biochemistry, 2008, v. 308 n. 1-2, p. 219-226en_US
dc.identifier.issn0300-8177en_US
dc.identifier.urihttp://hdl.handle.net/10722/163139-
dc.description.abstractEpithelial cell migration plays an important role in gastrointestinal mucosal repair. We previously reported that multiple functional ion channels, including a Ba2+-sensitive K+ inward rectifier Kir1.2, 4-aminopyridine (4-AP)-sensitive voltage-gated K+ channels Kv1.1, Kv1.6 and Kv2.1, and a nifedipine-sensitive, tetrodotoxin (TTX)-insensitive voltage-gated Na+ channel Nav1.5 were expressed in a non-transformed rat gastric epithelial cell line (RGM-1). In the present study, we further investigated whether these ion channels are involved in the modulation of gastric epithelial cell migration. Cell migration was determined by monolayer wound healing assay. Results showed that blockade of Kv with 4-AP or Nav1.5 with nifedipine inhibited RGM-1 cell migration in the absence or presence of epidermal growth factor (EGF), which effectively stimulated RGM-1 cell migration. Moreover, high concentration of TTX mimicked the action of nifedipine, suggesting that the action of nifedipine was mediated through specific blockade of Nav1.5. In contrast, inhibition of Kir1.2 with Ba2+, either in basal or EGF-stimulated condition, had no effect on RGM-1 cell migration. In conclusion, the present study demonstrates for the first time that voltage-gated K+ and Na+ channels are involved in the modulation of gastric epithelial cell migration. © Springer Science+Business Media, LLC. 2007.en_US
dc.languageengen_US
dc.publisherSpringer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0300-8177en_US
dc.relation.ispartofMolecular and Cellular Biochemistryen_US
dc.subject.mesh4-Aminopyridine - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBarium - Pharmacologyen_US
dc.subject.meshCell Lineen_US
dc.subject.meshCell Movement - Drug Effectsen_US
dc.subject.meshEpidermal Growth Factor - Pharmacologyen_US
dc.subject.meshEpithelial Cells - Cytology - Drug Effects - Metabolismen_US
dc.subject.meshGastric Mucosa - Cytology - Drug Effects - Metabolismen_US
dc.subject.meshGene Expression Regulation - Drug Effectsen_US
dc.subject.meshIon Channel Gating - Drug Effectsen_US
dc.subject.meshNifedipine - Pharmacologyen_US
dc.subject.meshPotassium Channel Blockers - Pharmacologyen_US
dc.subject.meshPotassium Channels, Voltage-Gated - Genetics - Metabolismen_US
dc.subject.meshRna, Messenger - Genetics - Metabolismen_US
dc.subject.meshRatsen_US
dc.subject.meshSodium Channel Blockers - Pharmacologyen_US
dc.subject.meshSodium Channels - Genetics - Metabolismen_US
dc.subject.meshTetrodotoxin - Pharmacologyen_US
dc.titleInvolvement of voltage-gated K+ and Na+ channels in gastric epithelial cell migrationen_US
dc.typeArticleen_US
dc.identifier.emailLi, GR:grli@hkucc.hku.hken_US
dc.identifier.authorityLi, GR=rp00476en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1007/s11010-007-9631-2en_US
dc.identifier.pmid17978865-
dc.identifier.scopuseid_2-s2.0-38649118553en_US
dc.identifier.hkuros146150-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-38649118553&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume308en_US
dc.identifier.issue1-2en_US
dc.identifier.spage219en_US
dc.identifier.epage226en_US
dc.identifier.isiWOS:000252637400027-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridWu, WKK=18345422600en_US
dc.identifier.scopusauthoridLi, GR=7408462932en_US
dc.identifier.scopusauthoridWong, TM=7403531434en_US
dc.identifier.scopusauthoridWang, JY=8438337300en_US
dc.identifier.scopusauthoridYu, L=7404164696en_US
dc.identifier.scopusauthoridCho, CH=14067000400en_US

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