Document Detail


Advanced glycation end product-induced apoptosis and overexpression of vascular endothelial growth factor and monocyte chemoattractant protein-1 in human-cultured mesangial cells.
MedLine Citation:
PMID:  11912219     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Advanced glycation end products (AGE) have been implicated in the pathogenesis of glomerulosclerosis in diabetes. However, their involvement in the development of the early phase of diabetic nephropathy has not been fully elucidated. We investigated the effects of AGE on growth and on vascular endothelial growth factor (VEGF) and monocyte chemoattractant protein-1 (MCP-1) expression in human cultured mesangial cells. We prepared three immunochemically distinct AGE by incubating bovine serum albumin (BSA) with glucose, glyceraldehyde, or glycolaldehyde. When human mesangial cells were cultured with various types of AGE-BSA, viable cell numbers as well as DNA syntheses were significantly decreased. All of the AGE-BSA were found to significantly increase p53 and Bax protein accumulations and subsequently induce apoptotic cell death in mesangial cells. An antioxidant, N-acetylcysteine, significantly prevented the AGE-induced apoptotic cell death in mesangial cells. Human mesangial cells stimulated prostacyclin production by co-cultured glomerular endothelial cells. Furthermore, various types of AGE-BSA were found to up-regulate the levels of mRNAs for VEGF and stimulate the secretion of VEGF and MCP-1 proteins in mesangial cells. The results suggest that AGE disturbed glomerular homeostasis by inducing apoptotic cell death in mesangial cells and elicited hyperfiltration and microalbuminuria by stimulating the secretion of VEGF and MCP-1 proteins, thereby being involved in the pathogenesis of the early phase of diabetic nephropathy.
Authors:
Sho-ichi Yamagishi; Yosuke Inagaki; Tamami Okamoto; Shinjiro Amano; Kohachiro Koga; Masayoshi Takeuchi; Zenji Makita
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2002-03-23
Journal Detail:
Title:  The Journal of biological chemistry     Volume:  277     ISSN:  0021-9258     ISO Abbreviation:  J. Biol. Chem.     Publication Date:  2002 Jun 
Date Detail:
Created Date:  2002-06-03     Completed Date:  2002-07-12     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  2985121R     Medline TA:  J Biol Chem     Country:  United States    
Other Details:
Languages:  eng     Pagination:  20309-15     Citation Subset:  IM    
Affiliation:
Division of Endocrinology and Metabolism, Department of Medicine, Kurume University School of Medicine, Kurume 830-0011, Japan. shoichi@med.kurume-u.ac.jp
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MeSH Terms
Descriptor/Qualifier:
Acetylcysteine / pharmacology
Apoptosis / physiology*
Cell Division
Cells, Cultured
Chemokine CCL2 / genetics*
Coculture Techniques
Diabetic Nephropathies / metabolism
Endothelial Growth Factors / genetics*
Glomerular Mesangium / cytology,  metabolism*
Glycosylation End Products, Advanced / physiology*
Humans
Lymphokines / genetics*
RNA, Messenger / genetics,  metabolism
Reverse Transcriptase Polymerase Chain Reaction
Tumor Suppressor Protein p53 / metabolism
Vascular Endothelial Growth Factor A
Vascular Endothelial Growth Factors
Chemical
Reg. No./Substance:
0/Chemokine CCL2; 0/Endothelial Growth Factors; 0/Glycosylation End Products, Advanced; 0/Lymphokines; 0/RNA, Messenger; 0/Tumor Suppressor Protein p53; 0/Vascular Endothelial Growth Factor A; 0/Vascular Endothelial Growth Factors; 616-91-1/Acetylcysteine

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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