File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Advanced-glycation-end-product-cholesterol-aggregated-protein accelerates the proliferation of mesangial cells mediated by transforming-growth-factor-beta 1 receptors and the ERK-MAPK pathway

TitleAdvanced-glycation-end-product-cholesterol-aggregated-protein accelerates the proliferation of mesangial cells mediated by transforming-growth-factor-beta 1 receptors and the ERK-MAPK pathway
Authors
Issue Date2011
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/ejphar
Citation
European Journal Of Pharmacology, 2011, v. 672 n. 1-3, p. 159-168 How to Cite?
AbstractHyperglycemia and hyperlipidemia are considered critical to the development of diabetic nephropathy. The aim of this study is to clarify the effect of cholesterol on advanced-glycation-end-products and the mechanisms behind the advanced-glycation-end-product-cholesterol-aggregated bovine serum albumin (BSA)-induced proliferation of mesangial cells. Mesangial cells were treated with advanced-glycation-end-product-cholesterol-aggregated-BSA, and RNA and protein were isolated. Cholesterol caused a 1.5-fold increase in fluorescent intensity and 2-fold increase in advanced-glycation-end-products in vitro. Pyridoxamine, aminoguanidine, and N-acetyl-l-cycteine suppressed the production of advanced-glycation-end-product-cholesterol-aggregated-BSA. Advanced-glycation-end-product-cholesterol-BSA was analyzed by matrix-assisted-laser-desorption/ionization-time of flight mass spectrometry, and peaks were found to shift toward a higher mass. Advanced-glycation-end- product-cholesterol-aggregated-BSA induced overexpression of the mRNA of transforming growth factor-beta1, collagen type 1, collagen type 4 and receptor for advanced-glycation-end-products, and the proliferation of mesangial cells. The injection of advanced-glycation-end-product-cholesterol-aggregated-BSA caused glomerular changes and albuminuria in non-diabetic mice. A transforming-growth-factor-beta receptor1 kinase inhibitor or Mitogen-activated-Protein-Kinase/Extracellular-Signal-regulated-Kinase kinase (ERK) inhibitor (U-0126) suppressed the proliferation of mesangial cells induced by advanced-glycation-end-product-cholesterol-aggregated-BSA dose-dependently. U-0126 inhibited the phosphorylation of ERK1/2 in advanced-glycation-end- product-cholesterol-aggregated-BSA treated mesangial cells. These findings suggested that cholesterol promotes the formation of advanced-glycation-end- products-protein and that advanced-glycation-end-product-cholesterol-aggregated protein stimulates mesangial cells to proliferate via transforming-growth- factor-beta receptors and the ERK-MAPK pathway in diabetic glomeruli. © 2011 Elsevier B.V. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/179462
ISSN
2015 Impact Factor: 2.73
2015 SCImago Journal Rankings: 1.115
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorHirasawa, Yen_US
dc.contributor.authorSakai, Ten_US
dc.contributor.authorIto, Men_US
dc.contributor.authorYoshimura, Hen_US
dc.contributor.authorFeng, Yen_US
dc.contributor.authorNagamatsu, Ten_US
dc.date.accessioned2012-12-19T09:56:48Z-
dc.date.available2012-12-19T09:56:48Z-
dc.date.issued2011en_US
dc.identifier.citationEuropean Journal Of Pharmacology, 2011, v. 672 n. 1-3, p. 159-168en_US
dc.identifier.issn0014-2999en_US
dc.identifier.urihttp://hdl.handle.net/10722/179462-
dc.description.abstractHyperglycemia and hyperlipidemia are considered critical to the development of diabetic nephropathy. The aim of this study is to clarify the effect of cholesterol on advanced-glycation-end-products and the mechanisms behind the advanced-glycation-end-product-cholesterol-aggregated bovine serum albumin (BSA)-induced proliferation of mesangial cells. Mesangial cells were treated with advanced-glycation-end-product-cholesterol-aggregated-BSA, and RNA and protein were isolated. Cholesterol caused a 1.5-fold increase in fluorescent intensity and 2-fold increase in advanced-glycation-end-products in vitro. Pyridoxamine, aminoguanidine, and N-acetyl-l-cycteine suppressed the production of advanced-glycation-end-product-cholesterol-aggregated-BSA. Advanced-glycation-end-product-cholesterol-BSA was analyzed by matrix-assisted-laser-desorption/ionization-time of flight mass spectrometry, and peaks were found to shift toward a higher mass. Advanced-glycation-end- product-cholesterol-aggregated-BSA induced overexpression of the mRNA of transforming growth factor-beta1, collagen type 1, collagen type 4 and receptor for advanced-glycation-end-products, and the proliferation of mesangial cells. The injection of advanced-glycation-end-product-cholesterol-aggregated-BSA caused glomerular changes and albuminuria in non-diabetic mice. A transforming-growth-factor-beta receptor1 kinase inhibitor or Mitogen-activated-Protein-Kinase/Extracellular-Signal-regulated-Kinase kinase (ERK) inhibitor (U-0126) suppressed the proliferation of mesangial cells induced by advanced-glycation-end-product-cholesterol-aggregated-BSA dose-dependently. U-0126 inhibited the phosphorylation of ERK1/2 in advanced-glycation-end- product-cholesterol-aggregated-BSA treated mesangial cells. These findings suggested that cholesterol promotes the formation of advanced-glycation-end- products-protein and that advanced-glycation-end-product-cholesterol-aggregated protein stimulates mesangial cells to proliferate via transforming-growth- factor-beta receptors and the ERK-MAPK pathway in diabetic glomeruli. © 2011 Elsevier B.V. All rights reserved.en_US
dc.languageengen_US
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/ejpharen_US
dc.relation.ispartofEuropean Journal of Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshButadienes - Pharmacologyen_US
dc.subject.meshCattleen_US
dc.subject.meshCell Proliferation - Drug Effectsen_US
dc.subject.meshCholesterol - Pharmacologyen_US
dc.subject.meshDiabetes Mellitus - Metabolism - Pathologyen_US
dc.subject.meshExtracellular Space - Drug Effects - Metabolismen_US
dc.subject.meshGlycosylation End Products, Advanced - Metabolismen_US
dc.subject.meshLipid Peroxidation - Drug Effectsen_US
dc.subject.meshMap Kinase Signaling System - Drug Effectsen_US
dc.subject.meshMaleen_US
dc.subject.meshMesangial Cells - Cytology - Drug Effects - Metabolism - Pathologyen_US
dc.subject.meshMiceen_US
dc.subject.meshMitogen-Activated Protein Kinase 1 - Metabolismen_US
dc.subject.meshMitogen-Activated Protein Kinase 3 - Metabolismen_US
dc.subject.meshMitogen-Activated Protein Kinases - Metabolismen_US
dc.subject.meshNitriles - Pharmacologyen_US
dc.subject.meshPhosphorylation - Drug Effectsen_US
dc.subject.meshProtein Multimerizationen_US
dc.subject.meshProtein Structure, Quaternaryen_US
dc.subject.meshRna, Messenger - Genetics - Metabolismen_US
dc.subject.meshReceptors, Transforming Growth Factor Beta - Metabolismen_US
dc.subject.meshSerum Albumin, Bovine - Chemistry - Metabolismen_US
dc.subject.meshTransforming Growth Factor Beta1 - Geneticsen_US
dc.titleAdvanced-glycation-end-product-cholesterol-aggregated-protein accelerates the proliferation of mesangial cells mediated by transforming-growth-factor-beta 1 receptors and the ERK-MAPK pathwayen_US
dc.typeArticleen_US
dc.identifier.emailFeng, Y: yfeng@hku.hken_US
dc.identifier.authorityFeng, Y=rp00466en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.ejphar.2011.09.185en_US
dc.identifier.pmid21989075-
dc.identifier.scopuseid_2-s2.0-81255160771en_US
dc.identifier.hkuros208638-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-81255160771&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume672en_US
dc.identifier.issue1-3en_US
dc.identifier.spage159en_US
dc.identifier.epage168en_US
dc.identifier.isiWOS:000298202700021-
dc.publisher.placeNetherlandsen_US
dc.identifier.scopusauthoridHirasawa, Y=7102854698en_US
dc.identifier.scopusauthoridSakai, T=7404830733en_US
dc.identifier.scopusauthoridIto, M=36981994100en_US
dc.identifier.scopusauthoridYoshimura, H=7402345484en_US
dc.identifier.scopusauthoridFeng, Y=24467969600en_US
dc.identifier.scopusauthoridNagamatsu, T=7006510058en_US
dc.identifier.citeulike9856236-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats