Bimodal Effect of Advanced Glycation End Products on Mesangial Cell Proliferation Is Mediated by Neutral Ceramidase Regulation and Endogenous Sphingolipids

Advanced glycation end-products (AGE) are generated by chronic hyperglycaemia and may cause diabetic microvascular complications such as diabetic nephropathy. Many factors influence the development of diabetic nephropathy; however, dysregulation of mesangial cell (MC) proliferation appears to play a...

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Bibliographic Details
Published in:The Journal of biological chemistry 2004-08, Vol.279 (33), p.34343-34352
Main Authors: Geoffroy, Karen, Wiernsperger, Nicolas, Lagarde, Michel, El Bawab, Samer
Format: Article
Language:English
Subjects:
Amidohydrolases - chemistry
Amidohydrolases - metabolism
Animals
Blotting, Western
Cell Division
Cells, Cultured
Ceramidases
Chromatography, High Pressure Liquid
Diabetes Mellitus, Experimental
Diacylglycerol Kinase - metabolism
Dose-Response Relationship, Drug
Gene Expression Regulation
Glomerular Mesangium - metabolism
Glucosylceramides - metabolism
Glycation End Products, Advanced - metabolism
Lysophospholipids - metabolism
Male
Models, Biological
Neutral Ceramidase
Phosphotransferases (Alcohol Group Acceptor) - metabolism
Rats
Rats, Wistar
Sphingolipids - metabolism
Sphingosine - analogs & derivatives
Sphingosine - metabolism
Thymidine - metabolism
Time Factors
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Summary:Advanced glycation end-products (AGE) are generated by chronic hyperglycaemia and may cause diabetic microvascular complications such as diabetic nephropathy. Many factors influence the development of diabetic nephropathy; however, dysregulation of mesangial cell (MC) proliferation appears to play an early and crucial role. In this study, we investigated the effects of AGE on rat MC proliferation and the involvement of sphingolipids in the AGE response. Results show a bimodal effect of AGE on MC proliferation. Thus, low AGE concentrations (
ISSN:0021-9258
1083-351X
DOI:10.1074/jbc.M403273200