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Growth factors modulate junctional cell-to-cell communication.
P E Maldonado1, B Rose, W R Loewenstein
1Department of Physiology and Biophysics, University of Miami School of Medicine, Florida 33101.
The Journal of Membrane Biology
|December 1, 1988
Summary
Epidermal growth factor (EGF) and platelet-derived growth factor (PDGF) reversibly inhibit cell communication by reducing gap junctional conductance. This early cellular response, dependent on EGF receptors, may play a role in growth regulation.
Area of Science:
- Cell Biology
- Molecular Biology
- Biochemistry
Background:
- Gap junctional communication is vital for cell-to-cell signaling.
- Growth factors like EGF and PDGF regulate cellular processes.
- Understanding growth factor effects on cell communication is crucial for cancer research.
Purpose of the Study:
- To investigate the effects of epidermal growth factor (EGF) and platelet-derived growth factor (PDGF) on gap junctional communication in mammalian cells.
- To determine the dose-dependency and reversibility of EGF and PDGF on cell communication.
- To explore the role of EGF receptors in mediating these effects.
Main Methods:
- Utilized mammalian cell lines (NRK and BalbC 3T3).
- Measured cell-to-cell transfer of a 400-dalton tracer molecule to assess communication.
- Quantified junctional conductance.
- Investigated the effects of varying concentrations of EGF and PDGF.
- Observed the time course of the response to EGF.
- Compared responses in normal cells versus EGF receptor-deficient cells (NIH 3T3).
Main Results:
- EGF and PDGF significantly inhibit gap junctional communication, reducing both tracer transfer and junctional conductance.
- The inhibition is dose-dependent and reversible.
- Half-maximal inhibition occurred at nanomolar concentrations for EGF and picomolar for PDGF.
- The response to EGF was rapid, detectable within 2 minutes and maximal within 10 minutes.
- EGF-induced inhibition was absent in EGF receptor-deficient NIH 3T3 cells.
- Transforming growth factor beta (TGF-β) enhanced communication in BalbC 3T3 cells but synergistically reduced it with EGF in NRK cells.
Conclusions:
- EGF and PDGF are potent inhibitors of mammalian cell gap junctional communication.
- The rapid and dose-dependent inhibition suggests a significant role in cellular regulation.
- EGF receptor presence is essential for EGF-mediated inhibition of gap junctional communication.
- TGF-β exhibits differential effects on cell communication depending on the cell type and presence of EGF receptors.