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- Publisher Website: 10.1016/j.ejphar.2011.09.185
- Scopus: eid_2-s2.0-81255160771
- PMID: 21989075
- WOS: WOS:000298202700021
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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
Title | 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 |
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Authors | |
Keywords | Advanced-glycation-end-product Cholesterol Diabetic nephropathy ERK-MAPK Mesangial cell |
Issue Date | 2011 |
Publisher | Elsevier 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? |
Abstract | Hyperglycemia 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 Identifier | http://hdl.handle.net/10722/179462 |
ISSN | 2023 Impact Factor: 4.2 2023 SCImago Journal Rankings: 1.055 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Hirasawa, Y | en_US |
dc.contributor.author | Sakai, T | en_US |
dc.contributor.author | Ito, M | en_US |
dc.contributor.author | Yoshimura, H | en_US |
dc.contributor.author | Feng, Y | en_US |
dc.contributor.author | Nagamatsu, T | en_US |
dc.date.accessioned | 2012-12-19T09:56:48Z | - |
dc.date.available | 2012-12-19T09:56:48Z | - |
dc.date.issued | 2011 | en_US |
dc.identifier.citation | European Journal Of Pharmacology, 2011, v. 672 n. 1-3, p. 159-168 | en_US |
dc.identifier.issn | 0014-2999 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/179462 | - |
dc.description.abstract | Hyperglycemia 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.language | eng | en_US |
dc.publisher | Elsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/ejphar | en_US |
dc.relation.ispartof | European Journal of Pharmacology | en_US |
dc.subject | Advanced-glycation-end-product | - |
dc.subject | Cholesterol | - |
dc.subject | Diabetic nephropathy | - |
dc.subject | ERK-MAPK | - |
dc.subject | Mesangial cell | - |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Butadienes - Pharmacology | en_US |
dc.subject.mesh | Cattle | en_US |
dc.subject.mesh | Cell Proliferation - Drug Effects | en_US |
dc.subject.mesh | Cholesterol - Pharmacology | en_US |
dc.subject.mesh | Diabetes Mellitus - Metabolism - Pathology | en_US |
dc.subject.mesh | Extracellular Space - Drug Effects - Metabolism | en_US |
dc.subject.mesh | Glycosylation End Products, Advanced - Metabolism | en_US |
dc.subject.mesh | Lipid Peroxidation - Drug Effects | en_US |
dc.subject.mesh | Map Kinase Signaling System - Drug Effects | en_US |
dc.subject.mesh | Male | en_US |
dc.subject.mesh | Mesangial Cells - Cytology - Drug Effects - Metabolism - Pathology | en_US |
dc.subject.mesh | Mice | en_US |
dc.subject.mesh | Mitogen-Activated Protein Kinase 1 - Metabolism | en_US |
dc.subject.mesh | Mitogen-Activated Protein Kinase 3 - Metabolism | en_US |
dc.subject.mesh | Mitogen-Activated Protein Kinases - Metabolism | en_US |
dc.subject.mesh | Nitriles - Pharmacology | en_US |
dc.subject.mesh | Phosphorylation - Drug Effects | en_US |
dc.subject.mesh | Protein Multimerization | en_US |
dc.subject.mesh | Protein Structure, Quaternary | en_US |
dc.subject.mesh | Rna, Messenger - Genetics - Metabolism | en_US |
dc.subject.mesh | Receptors, Transforming Growth Factor Beta - Metabolism | en_US |
dc.subject.mesh | Serum Albumin, Bovine - Chemistry - Metabolism | en_US |
dc.subject.mesh | Transforming Growth Factor Beta1 - Genetics | en_US |
dc.title | 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 | en_US |
dc.type | Article | en_US |
dc.identifier.email | Feng, Y: yfeng@hku.hk | en_US |
dc.identifier.authority | Feng, Y=rp00466 | en_US |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.doi | 10.1016/j.ejphar.2011.09.185 | en_US |
dc.identifier.pmid | 21989075 | - |
dc.identifier.scopus | eid_2-s2.0-81255160771 | en_US |
dc.identifier.hkuros | 208638 | - |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-81255160771&selection=ref&src=s&origin=recordpage | en_US |
dc.identifier.volume | 672 | en_US |
dc.identifier.issue | 1-3 | en_US |
dc.identifier.spage | 159 | en_US |
dc.identifier.epage | 168 | en_US |
dc.identifier.isi | WOS:000298202700021 | - |
dc.publisher.place | Netherlands | en_US |
dc.identifier.scopusauthorid | Hirasawa, Y=7102854698 | en_US |
dc.identifier.scopusauthorid | Sakai, T=7404830733 | en_US |
dc.identifier.scopusauthorid | Ito, M=36981994100 | en_US |
dc.identifier.scopusauthorid | Yoshimura, H=7402345484 | en_US |
dc.identifier.scopusauthorid | Feng, Y=24467969600 | en_US |
dc.identifier.scopusauthorid | Nagamatsu, T=7006510058 | en_US |
dc.identifier.citeulike | 9856236 | - |
dc.identifier.issnl | 0014-2999 | - |