May 2005
Volume 46, Issue 13
ARVO Annual Meeting Abstract  |   May 2005
UVB Activated Pathways in Pterygium Pathogenesis
Author Affiliations & Notes
  • M.T. Coroneo
    Department of Ophthalmology, UNSW Prince of Wales Hospital, Sydney, Australia
  • N. Di Girolamo
    Pathology, University of New South Wales, Sydney, Australia
  • D. Wakefield
    Pathology, University of New South Wales, Sydney, Australia
  • Footnotes
    Commercial Relationships  M.T. Coroneo, None; N. Di Girolamo, None; D. Wakefield, None.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 963. doi:
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      M.T. Coroneo, N. Di Girolamo, D. Wakefield; UVB Activated Pathways in Pterygium Pathogenesis . Invest. Ophthalmol. Vis. Sci. 2005;46(13):963.

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

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Abstract: : Purpose: A central process in pterygium pathogenesis is thought to be matrix metalloproteinase (MMP) activation by ultraviolet light (UV) and subsequent MMP activity against interstitial tissue. A number of MMP’s are involved but MMP–1 is abundantly expressed in pterygia. The purpose of this study was to identify the pathways responsible for the enhanced expression of MMP–1 in pterygium epithelial cells (PEC) following UVB exposure and to determine whether cell–surface receptors transmit the UV stress signal. Methods: : Immunohistochemical analysis was performed on diseased and normal ocular tissue. PEC were cultured and exposed to UVB and/or treated with inhibitors of mitogen activated protein kinase (MAPK), pertussis toxin or an epidermal growth factor receptor (EGFR) inhibitor. Conditioned medium and cell lysates were analyzed by gelatin zymography, Western blotting, and ELISA. Total RNA was reverse transcribed and analyzed by PCR. Results: MMP–1 protein was strongly expressed in pterygium specimens compared to normal conjunctiva, limbus, and cornea. The UVB–mediated induction of MMP–1 was completely inhibited following the treatment of PEC with PD98059, a specific ERK1/2 MAPK inhibitor. SB203580, an inhibitor of JNK and p38 was not able to reduce the production of MMP–1. UVB radiation increased levels of phosphorylated ERK1/2 in a time–dependent manner and the addition of PD98059 decreased this induction by at least 12–fold. c–fos transcripts were detected as early as 2–hrs, returned to basal levels 24–hrs post–UVB and were inhibited by PD98059 in cultured PEC. Immunohistochemical analysis revealed both total and active/phosphorylated EGFR in pterygium tissue and in UVB irradiated PEC. Pertussis toxin reduced the UVB–mediated induction of MMP–1 in PEC by at least 30% suggesting the involvement of a G–protein coupled receptor and PD153035 (a specific EGFR inhibitor) had a similar effect. Conclusions: A UV sensitive cell–surface receptor and a specific intracellular signaling pathway responsible for the enhanced production of a key enzyme that denatures corneal collagens have been demonstrated. These results advance our knowledge as to how pterygia may develop and may allow consideration of non–surgical strategies to treat this disease.

Keywords: Pterygium • signal transduction • radiation damage: light/UV 

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