Skip to main content
padlock icon - secure page this page is secure

Open Access Captopril-dependent inhibition of collagen biosynthesis in cultured fibroblasts

Download Article:
(PDF 250.9 kb)
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 48 h. 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 1 integrin signaling, the effect of CAP on IGF-IR and 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, α21 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 α21 integrin and IGF-IR signaling.
No References for this article.
No Supplementary Data.
No Article Media
No Metrics

Document Type: Research Article

Publication date: August 1, 2010

More about this publication?
  • Pharmazie is a leading journal in the field of pharmaceutical sciences. As a peer-reviewed scientific journal, Pharmazie is regularly indexed in the relevant databases like Web of science, Journal Citation Reports and many others. The journal is open for submissions from the whole spectrum of pharnaceutical sciences including Pharmaceutical Chemistry, Experimental and Clinical Pharmacology, Drug Analysis, Pharmaceutics, Pharmaceutical Biology, Clinical Pharmacy etc.
  • Information for Authors
  • Submit a Paper
  • Subscribe to this Title
  • Ingenta Connect is not responsible for the content or availability of external websites
  • Access Key
  • Free content
  • Partial Free content
  • New content
  • Open access content
  • Partial Open access content
  • Subscribed content
  • Partial Subscribed content
  • Free trial content
Cookie Policy
Cookie Policy
Ingenta Connect website makes use of cookies so as to keep track of data that you have filled in. I am Happy with this Find out more