Regulation of endothelial IGFBP-3 synthesis and secretion by IGF-I and TGF-beta

Growth Regul. 1996 Mar;6(1):1-9.

Abstract

We have examined the regulation of endothelial IGFBP-3 production by IGF-I and TGF-beta, two growth factors thought to play a major roles in the complications of diabetes mellitus. In addition, we developed a sensitive method for IGFBP-3 mRNA quantitation by adapting the fluorescent modification of the competitive PCR strategy. Our results using both Northern analysis and the fluorescent competitive PCR method indicate that: (1) IGFBP-3 mRNA is increased 2- to 10-fold by IGF-I and maximally reduced to 20% of control by TGF-beta; (2) the changes in mRNA levels correlate with the levels of IGFBP-3 protein secreted into the media by these cells; (3) the induction of IGFBP-3 mRNA and protein by IGF-I analogs was directly related to their ability to bind to the type I IGF receptor, reflecting an IGF-I receptor-mediated process; and (4) steady state IGFBP-3 mRNA levels did not change significantly after a 6 h incubation with actinomycin D in the presence or absence of the growth factors suggesting that the observed IGF-I/TGF-beta effects occur at the level of gene transcription rather than mRNA stability.

Publication types

  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adipose Tissue
  • Animals
  • Aorta
  • Base Sequence
  • Blotting, Northern
  • Cattle
  • Cells, Cultured
  • DNA Primers
  • Endothelium, Vascular / drug effects
  • Endothelium, Vascular / metabolism*
  • Gene Expression Regulation / drug effects
  • Insulin-Like Growth Factor Binding Protein 3 / biosynthesis*
  • Insulin-Like Growth Factor I / analogs & derivatives
  • Insulin-Like Growth Factor I / metabolism
  • Insulin-Like Growth Factor I / pharmacology*
  • Molecular Sequence Data
  • Polymerase Chain Reaction
  • RNA, Messenger / analysis
  • RNA, Messenger / biosynthesis
  • Receptor, IGF Type 1 / drug effects
  • Receptor, IGF Type 1 / physiology
  • Transcription, Genetic / drug effects*
  • Transforming Growth Factor beta / pharmacology*

Substances

  • DNA Primers
  • Insulin-Like Growth Factor Binding Protein 3
  • RNA, Messenger
  • Transforming Growth Factor beta
  • Insulin-Like Growth Factor I
  • Receptor, IGF Type 1