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Angiogenic response of advanced glycation end products (AGEs) involves PPAR <sub><img src='/image/spc_char/gamma2.gif' border=0></sub>

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Title Angiogenic response of advanced glycation end products (AGEs) involves PPAR
 
Creator Devi, Manju S
Sudhakaran, Perumana R
 
Subject Advanced Glycation End Products (AGE s)
PPAR
Angiogenesis
Diabetes
VEGF
 
Description 18-24
Diabetes
is associated with increased formation of advanced glycation end products
(AGEs), which have been implicated in micro and macrovascular complications of
diabetes. Our earlier reports showed proangiogenic effect of
AGE-bovine serum albumin (BSA). In order to understand the mechanism of
AGE-mediated angiogenesis, the possibility of involvement of peroxisome
prolifeator activated receptor (PPAR) , a ligand
activated transcription factor was examined. The angiogenic effect was
studied in chick chorio allantoic membrane (CAM)
and by analyzing angiogenic markers in human umbilical vein endothelial cells
(HUVECs) in culture. The involvement of PPAR was investigated
using synthetic PPAR agonist GW 1929 and antagonist GW 9662 and by RT-PCR. In CAM
assay, PPAR antagonist GW 9662 reversed the
AGE-induced effect on vascularity. In HUVECs in culture, GW 9662
reversed the effect of AGE-BSA and decreased the expression of CD 31,
E-Selectin and VEGF. RT-PCR analysis showed that treatment with AGE-BSA caused
upregulation
of PPAR mRNA levels. The reversal of the
effect of AGE on angiogenesis by treatment with PPAR
antagonists and
up-regulation of PPAR gene in HUVECs treated
with AGE-BSA suggested the possible involvement of PPAR
-dependent downstream pathway in mediating the angiogenic effect of
AGE.
 
Date 2012-02-14T12:26:19Z
2012-02-14T12:26:19Z
2012-02
 
Type Article
 
Identifier 0975-0959 (Online); 0301-1208 (Print)
http://hdl.handle.net/123456789/13587
 
Language en_US
 
Rights CC Attribution-Noncommercial-No Derivative Works 2.5 India
 
Publisher NISCAIR-CSIR, India
 
Source IJBB Vol.49(1) [February 2012]