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Bradykinin-induced growth inhibition of normal rat kidney (NRK) cells is paralleled by a decrease in
E J Van Zoelen1, P H Peters, G B Afink
1Department of Cell Biology, University of Nijmegen, Faculty of Science, The Netherlands.
The Biochemical Journal
|March 1, 1994
Summary
Bradykinin prevents growth factor-induced loss of cell cycle arrest in fibroblasts. This receptor-mediated mechanism specifically blocks transforming growth factor beta and retinoic acid effects, impacting epidermal growth factor receptor levels.
Area of Science:
- Cell biology
- Molecular endocrinology
- Cancer research
Background:
- Normal rat kidney fibroblasts exhibit density-dependent growth arrest.
- Epidermal growth factor (EGF) is present during this arrest.
- Phenotypic transformation can be induced by transforming growth factor beta (TGF-β) or retinoic acid (RA).
Purpose of the Study:
- To investigate the effect of bradykinin on growth stimulus-induced loss of density-dependent growth arrest.
- To determine the mechanism of bradykinin's action.
- To examine bradykinin's effect on epidermal growth factor (EGF) receptor levels.
Main Methods:
- Treatment of density-arrested rat kidney fibroblasts with bradykinin, TGF-β, RA, and prostaglandin F2 alpha.
- Northern-blot analysis to assess gene expression.
- Receptor-binding studies to quantify receptor levels.
Main Results:
- Bradykinin specifically blocks the loss of density-dependent growth arrest induced by TGF-β or RA.
- Bradykinin's effect is receptor-mediated and not mimicked by prostaglandin F2 alpha.
- Bradykinin inhibits the RA-induced increase in EGF receptor levels.
Conclusions:
- Bradykinin acts via a specific receptor-mediated mechanism to maintain density-dependent growth arrest.
- Bradykinin influences EGF receptor levels, suggesting a role in modulating EGF-induced cell transformation.
- These findings highlight a novel regulatory pathway in fibroblast growth control.