Captopril-dependent inhibition of collagen biosynthesis in cultured fibroblasts

被引：11

作者：

Karna, E. ^{[1
]}

Szoka, L. ^{[1
]}

Palka, J. A. ^{[1
]}

机构：

[1] Med Univ Bialystok, Dept Med Chem, PL-15089 Bialystok, Poland

来源：

PHARMAZIE | 2010年 / 65卷 / 08期

关键词：

HUMAN-SKIN FIBROBLASTS; GROWTH-FACTOR-I; CONVERTING ENZYME-INHIBITOR; PROLIDASE ACTIVITY; EXTRACELLULAR-MATRIX; PROLINE; INSULIN; IMINODIPEPTIDURIA; DIFFERENTIATION; PROCOLLAGEN;

D O I：

10.1691/ph.2010.9844

中图分类号：

R914 [药物化学];

学科分类号：

100701 ;

摘要：

The mechanism underlying the dermatological manifestations that accompany captopril therapy is not known. The facts that prolidase plays an important role in collagen biosynthesis and that captopril directly inhibits prolidase activity led us to evaluate its effect on collagen biosynthesis in cultured human skin fibroblasts. Confluent fibroblasts were treated with milimolar concentrations (0.2-1 mM) of captopril (CAP) for 48h. It was found that CAP-dependent decrease in prolidase activity was accompanied by parallel decrease in collagen biosynthesis. Since insulin-like growth factor receptor (IGF-IR) is the most potent regulator of both collagen biosynthesis and prolidase activity, and prolidase is regulated by beta(1) integrin signaling, the effect of CAP on IGF-IR and beta(1) integrin receptor expressions was evaluated. It was found that exposure of the cells to 0.3 mM CAP contributed to a decrease in IGF-IR, alpha(2)beta(1) integrin receptor and MAPK/ ERK1/2 expressions. The data suggest that CAP-dependent decrease of collagen biosynthesis in cultured human skin fibroblasts results from inhibition of prolidase activity that may occur through inhibition of alpha(2)beta(1) integrin and IGF-IR signaling.

引用

页码：614 / 617

页数：4

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