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Conference Paper: Lipopolysaccharide impairs gap junction function and reduces rat kidney NRK-52E cell proliferation

TitleLipopolysaccharide impairs gap junction function and reduces rat kidney NRK-52E cell proliferation
Authors
KeywordsBiology
Issue Date2012
PublisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/
Citation
Experimental Biology Annual Meeting (EB 2012), San Diego, CA., 21-25 April 2012. In The FASEB Journal, 2012, v. 26 Meeting abstracts suppl., abstract no. 1051.11 How to Cite?
AbstractEndotoxin lipopolysaccharide (LPS)-induced shock is life-threatening which is often associated with acute renal failure. Gap junctions (GJ) play critical roles in maintaining kidney functions by facilitating intercellular communication and tubular purinergic signaling. However, it is unknown whether or not LPS may cause acute kidney injury by impairing renal GJ functions. Renal tubular epithelial cells are one of the main parenchymal cells that are susceptible to injurious stimuli. We, therefore, employed normal rat renal tubular epithelial cell line (NRK-52E) to investigate the impact of LPS on cell proliferation and GJ function. NRK-52E cells were seeded at high and low density to promote or impede GJ formation, respectively, and to establish distinctive levels of intercellular communication We found that LPS dose-dependently reduced cell proliferation rate and colony-formation rate of high and low density NRK-52E cells when LPS concentration was above 100 ng/mL, accompanied with reduced connexin43 protein expression and reduced fluorescent dye transmission between adjacent cells (all p<0.05 vs. control without LPS stimulation). The GJ inhibitor oleamide attenuated LPS-induced reduction in colony-formation rate of high density cells, but further decreased fluorescent transmission (all P<0.05 vs. LPS). In contrast, GJ agonist retinoic acid increased fluorescent dye transmission. It is concluded that impairment in GJ function may represent a mechanism whereby LPS induces kidney cell injury.
DescriptionOpen Access Journal
Persistent Identifierhttp://hdl.handle.net/10722/160566
ISSN
2014 Impact Factor: 5.043
2014 SCImago Journal Rankings: 2.516

 

DC FieldValueLanguage
dc.contributor.authorWang, Yen_US
dc.contributor.authorWei, Jen_US
dc.contributor.authorXia, Zen_US
dc.contributor.authorHei, Zen_US
dc.contributor.authorLuo, Cen_US
dc.date.accessioned2012-08-16T06:14:24Z-
dc.date.available2012-08-16T06:14:24Z-
dc.date.issued2012en_US
dc.identifier.citationExperimental Biology Annual Meeting (EB 2012), San Diego, CA., 21-25 April 2012. In The FASEB Journal, 2012, v. 26 Meeting abstracts suppl., abstract no. 1051.11en_US
dc.identifier.issn0892-6638-
dc.identifier.urihttp://hdl.handle.net/10722/160566-
dc.descriptionOpen Access Journal-
dc.description.abstractEndotoxin lipopolysaccharide (LPS)-induced shock is life-threatening which is often associated with acute renal failure. Gap junctions (GJ) play critical roles in maintaining kidney functions by facilitating intercellular communication and tubular purinergic signaling. However, it is unknown whether or not LPS may cause acute kidney injury by impairing renal GJ functions. Renal tubular epithelial cells are one of the main parenchymal cells that are susceptible to injurious stimuli. We, therefore, employed normal rat renal tubular epithelial cell line (NRK-52E) to investigate the impact of LPS on cell proliferation and GJ function. NRK-52E cells were seeded at high and low density to promote or impede GJ formation, respectively, and to establish distinctive levels of intercellular communication We found that LPS dose-dependently reduced cell proliferation rate and colony-formation rate of high and low density NRK-52E cells when LPS concentration was above 100 ng/mL, accompanied with reduced connexin43 protein expression and reduced fluorescent dye transmission between adjacent cells (all p<0.05 vs. control without LPS stimulation). The GJ inhibitor oleamide attenuated LPS-induced reduction in colony-formation rate of high density cells, but further decreased fluorescent transmission (all P<0.05 vs. LPS). In contrast, GJ agonist retinoic acid increased fluorescent dye transmission. It is concluded that impairment in GJ function may represent a mechanism whereby LPS induces kidney cell injury.-
dc.languageengen_US
dc.publisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/-
dc.relation.ispartofThe FASEB Journalen_US
dc.subjectBiology-
dc.titleLipopolysaccharide impairs gap junction function and reduces rat kidney NRK-52E cell proliferationen_US
dc.typeConference_Paperen_US
dc.identifier.emailXia, Z: zyxia@hkucc.hku.hken_US
dc.identifier.authorityXia, Z=rp00532en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.hkuros205208en_US
dc.identifier.volume26en_US
dc.identifier.issueMeeting abstracts suppl.-
dc.identifier.spageabstract no. 1051.11en_US
dc.identifier.epageabstract no. 1051.11en_US
dc.publisher.placeUnited States-
dc.description.otherExperimental Biology Annual Meeting (EB 2012), San Diego, CA., 21-25 April 2012. In The FASEB Journal, 2012, v. 26 Meeting abstracts suppl., abstract no. 1051.11-

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