December 2002
Volume 43, Issue 13
Free
ARVO Annual Meeting Abstract  |   December 2002
Epidermal Growth Factor Activation Of Extracellular Signal-Regulated Protein Kinases In Human Corneal Epithelial Cells
Author Affiliations & Notes
  • Z Wang
    Biological Sciences SUNY College of Optometry New York NY
  • VN Bildin
    Biological Sciences SUNY College of Optometry New York NY
  • PS Reinach
    Biological Sciences SUNY College of Optometry New York NY
  • Footnotes
    Commercial Relationships   Z. Wang, None; V.N. Bildin, None; P.S. Reinach, None. Grant Identification: NIH Grant EY04795 and the SIVR Foundation.
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 1653. doi:
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      Z Wang, VN Bildin, PS Reinach; Epidermal Growth Factor Activation Of Extracellular Signal-Regulated Protein Kinases In Human Corneal Epithelial Cells . Invest. Ophthalmol. Vis. Sci. 2002;43(13):1653.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Abstract: : Purpose: Activation of extracellular signal-regulated protein kinase (Erk1/2) is essential for corneal epithelial mitogenesis. We investigated in SV40-immortalized human corneal epithelial cells (HCEC) the relative roles of protein kinase C (PKC) stimulation and tyrosine kinase phosphorylation on the ability of EGF to activate cRaf, Erk and stimulate Elk-1 gene transcription factor as well as induce mitogenesis. Methods: After 24 h incubation without serum, HCEC proliferation was stimulated with 10 ng/ml EGF. The contribution of protein tyrosine phosphorylation steps to Erk activation was evaluated with PD153035 (EGF receptor tyrosine kinase inhibitor) and manumycin A (Ras farnesyltransferase inhibitor). EGF-induced PKC activation was inhibited with bisindolylmaleimide. Levels of cRaf, Erk1/2 and Elk-1 activation were determined by Western blotting/ECL assay 30 min after EGF exposure. Cell proliferation was determined based on measurements of 3H-thymidine incorporation after 20 h. Results: PKC inhibition during serum starvation produced up to a 20% increase in proliferation, but it had no significant effect on the mitogenic response to EGF. Surprisingly PKC inhibition in the presence of EGF caused moderate decreases in cRaf and Erk1/2 activity. On the other hand, inhibition of EGF receptor and cytosolic associated tyrosine kinase phosphorylation dramatically (5-10-fold) decreased Erk1/2 and Elk-1 activation and nearly completely inhibited the mitogenic response to EGF. Conclusion: In HCEC, EGF-induced Erk1/2 stimulation and its mitogenic effect are only partially dependent on the activation of PKC by EGF. This is in contrast to the findings in some other cell types in which there is a greater dependency of these EGF associated responses on PKC activation. On the other hand, EGF-induced EGF receptor and cytosolic associated tyrosine kinase phosphorylation is essential for EGF-induced Erk activation and its stimulation of proliferation.

Keywords: 423 growth factors/growth factor receptors • 399 enzymes/enzyme inhibitors • 372 cornea: epithelium 
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