August 1989
Volume 30, Issue 8
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Articles  |   August 1989
EGF does not enhance corneal epithelial cell motility.
Author Affiliations
  • H K Soong
    Department of Ophthalmology, University of Michigan Medical School, Ann Arbor.
  • B McClenic
    Department of Ophthalmology, University of Michigan Medical School, Ann Arbor.
  • J Varani
    Department of Ophthalmology, University of Michigan Medical School, Ann Arbor.
  • T Hassan
    Department of Ophthalmology, University of Michigan Medical School, Ann Arbor.
  • S C Huang
    Department of Ophthalmology, University of Michigan Medical School, Ann Arbor.
  • R Brenz
    Department of Ophthalmology, University of Michigan Medical School, Ann Arbor.
Investigative Ophthalmology & Visual Science August 1989, Vol.30, 1808-1812. doi:
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    • Get Citation

      H K Soong, B McClenic, J Varani, T Hassan, S C Huang, R Brenz; EGF does not enhance corneal epithelial cell motility.. Invest. Ophthalmol. Vis. Sci. 1989;30(8):1808-1812.

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

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Abstract

Although it is well known that epidermal growth factor (EGF) accelerates corneal epithelial wound healing by stimulating mitosis, it is also believed that EGF may directly stimulate the motility of individual corneal epithelial cells. We employed three different experimental methods to determine if EGF does indeed enhance the motility of corneal epithelial cells (independent of mitotic effects). First, the effects of EGF on the motility of tissue-cultured rat and rabbit corneal epithelial cells were investigated by a Boyden chamber assay. In rat corneal epithelium, these effects were further investigated by a second method, the agarose drop assay. Both assay techniques demonstrated no increase in corneal epithelial cell motility in the presence of EGF. These findings were corroborated by a third method which consisted of measuring the closure rate of epithelial wounds in organ-cultured rat corneas in the presence and absence of EGF, while concurrently arresting mitosis with colchicine. The wound closure rate before addition of any drug was 0.46 +/- 0.03 mm2/hr. The wound closure rate with EGF (50 ng/ml) was 0.55 +/- 0.03 mm2/hr, significantly (P less than 0.005) more rapid than the drug-free controls. However, when EGF (50 ng/ml) and colchicine (40 micrograms/ml) were used simultaneously, the acceleration of wound closure by EGF was completely negated by the presence of colchicine, resulting in a wound closure rate (0.46 +/- 0.06 mm2/hr) that did not differ significantly (P greater than 0.50) from that of the drug-free control.(ABSTRACT TRUNCATED AT 250 WORDS)

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