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Updated: Oct 2, 2026

Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling
07:49

Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling

Published on: August 3, 2018

Autocrine production of basic fibroblast growth factor translated from novel synthesized mRNA mediates

Alessandra Cucina1, Valeria Borrelli, Marco Lucarelli

  • 1First Department of Surgery, University of Rome La Sapienza, Rome, Italy. acucina@uniroma1.it

Cell Biochemistry and Function
|February 9, 2002
PubMed

Insights

Thrombin stimulates smooth muscle cell (SMC) growth partly through autocrine basic fibroblast growth factor (bFGF) production. This involves new mRNA synthesis and translation, contributing to SMC proliferation.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Thrombin is known to stimulate smooth muscle cell (SMC) growth in culture.
  • Previous studies indicate thrombin increases platelet-derived growth factor AA and basic fibroblast growth factor (bFGF) release by SMCs.
  • The precise mechanisms linking thrombin, bFGF, and SMC proliferation are not fully understood.

Purpose of the Study:

  • To clarify the link between thrombin, bFGF, and SMC proliferation.
  • To examine the kinetics of autocrine bFGF production by thrombin-stimulated SMCs.
  • To determine the contribution of autocrine bFGF to thrombin-induced mitogenesis.

Main Methods:

  • Bovine aortic SMCs were stimulated with thrombin in serum-free culture.
  • bFGF mRNA expression was analyzed using RT-PCR.
  • Mitogenic activity was assessed by 3H-thymidine uptake.
  • Experiments utilized cycloheximide (translation inhibitor) and anti-bFGF antibody, and hirudin (thrombin inhibitor).

Main Results:

  • Peak bFGF mRNA expression occurred 24 hours after thrombin stimulation.
  • Translation of bFGF occurred later than 24 hours post-stimulation, as indicated by cycloheximide experiments.
  • Thrombin-induced SMC mitogenic activity was partially inhibited by anti-bFGF antibody and hirudin.
  • Inhibition was not observed when hirudin was added 24 hours after stimulation, suggesting a time-dependent role for thrombin.

Conclusions:

  • Thrombin-induced SMC mitogenesis is partially mediated by autocrine bFGF production.
  • This process primarily involves protein synthesis from novel mRNA, with transcription peaking at 24 hours and translation occurring later.
  • The findings elucidate a key pathway in thrombin-mediated SMC growth regulation.

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