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Conference Paper: Lipopolysaccharide impairs gap junction function and reduces rat kidney NRK-52E cell proliferation
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TitleLipopolysaccharide impairs gap junction function and reduces rat kidney NRK-52E cell proliferation
 
AuthorsWang, Y
Wei, J
Xia, Z
Hei, Z
Luo, C
 
KeywordsBiology
 
Issue Date2012
 
PublisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/
 
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. 1051.11 [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
 
ISSN0892-6638
2013 Impact Factor: 5.480
 
DC FieldValue
dc.contributor.authorWang, Y
 
dc.contributor.authorWei, J
 
dc.contributor.authorXia, Z
 
dc.contributor.authorHei, Z
 
dc.contributor.authorLuo, C
 
dc.date.accessioned2012-08-16T06:14:24Z
 
dc.date.available2012-08-16T06:14:24Z
 
dc.date.issued2012
 
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.description.naturelink_to_OA_fulltext
 
dc.descriptionOpen Access Journal
 
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
 
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. 1051.11 [How to Cite?]
 
dc.identifier.epageabstract no. 1051.11
 
dc.identifier.hkuros205208
 
dc.identifier.issn0892-6638
2013 Impact Factor: 5.480
 
dc.identifier.issueMeeting abstracts suppl.
 
dc.identifier.spageabstract no. 1051.11
 
dc.identifier.urihttp://hdl.handle.net/10722/160566
 
dc.identifier.volume26
 
dc.languageeng
 
dc.publisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/
 
dc.publisher.placeUnited States
 
dc.relation.ispartofThe FASEB Journal
 
dc.subjectBiology
 
dc.titleLipopolysaccharide impairs gap junction function and reduces rat kidney NRK-52E cell proliferation
 
dc.typeConference_Paper
 
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