RECEPTOR-MEDIATED TOXICITY TO PERICYTES OF ADVANCED GLYCOSYLATION END-PRODUCTS - A POSSIBLE MECHANISM OF PERICYTE LOSS IN DIABETIC MICROANGIOPATHY

被引：133

作者：

YAMAGISHI, SI

HSU, CC

TANIGUCHI, M

HARADA, SI

YAMAMOTO, Y

OHSAWA, KS

KOBAYASHI, KI

YAMAMOTO, H

机构：

[1] KANAZAWA UNIV,SCH MED,DEPT BIOCHEM,KANAZAWA,ISHIKAWA 920,JAPAN

[2] KANAZAWA UNIV,SCH MED,DEPT INTERNAL MED 1,KANAZAWA,ISHIKAWA 920,JAPAN

[3] CHUNG SHAN MED & DENT COLL,TAICHUNG,TAIWAN

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 1995年 / 213卷 / 02期

关键词：

D O I：

10.1006/bbrc.1995.2185

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The influence of advanced glycosylation end products (AGE) on bovine retinal pericytes was investigated. When pericytes were cultured with AGE-bovine serum albumin (BSA), pericyte growth was significantly retarded in a dose-dependent manner. They also exhibited an immediate toxicity to pericytes. However, MRC-5 human fibroblasts were totally resistant to AGE-BSA. Moreover, antisense oligonucleotides complementary to mRNA coding for AGE receptor were found to reverse the AGE-induced decrease in viable pericyte number, although the mRNA level was about one order of magnitude lower in pericytes than in the fibroblasts. These results indicate that pericytes may possess a peculiar sensitivity to AGE, and that AGE ligand-receptor interactions may play an important role in the pathogenesis of pericyte loss, the principal change in diabetic microangiopathies. (C) 1995 Academic Press, Inc.

引用

页码：681 / 687

页数：7

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