April 2009
Volume 50, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2009
MAP Kinase Signaling Pathway in Human Corneal and Conjunctival Epithelial Cells
Author Affiliations & Notes
  • M. Massaro-Giordano
    Ophthalmology, Scheie Eye Institute, Philadelphia, Pennsylvania
  • M. Montanari
    College of Science and Technology, Temple University/ Sbarro Institute for Cancer Research and Molecular Medicine, Philadelphia, Pennsylvania
  • C. M. Marshall
    Dermatology, University of Pennsylvania, Philadelphia, Pennsylvania
  • A. Giordano
    College of Science and Technology, Temple University/ Sbarro Institute for Cancer Research and Molecular Medicine, Philadelphia, Pennsylvania
  • M. Macaluso
    College of Science and Technology, Temple University/ Sbarro Institute for Cancer Research and Molecular Medicine, Philadelphia, Pennsylvania
  • Footnotes
    Commercial Relationships  M. Massaro-Giordano, None; M. Montanari, None; C.M. Marshall, None; A. Giordano, None; M. Macaluso, None.
  • Footnotes
    Support  Sbarro Health Research Organization
Investigative Ophthalmology & Visual Science April 2009, Vol.50, 4630. doi:
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      M. Massaro-Giordano, M. Montanari, C. M. Marshall, A. Giordano, M. Macaluso; MAP Kinase Signaling Pathway in Human Corneal and Conjunctival Epithelial Cells. Invest. Ophthalmol. Vis. Sci. 2009;50(13):4630.

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

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Abstract

Purpose: : Plasminogen Activator Inhibitor Type 2 (PAI-2) is a multifunctional protein found in various cell types. Previously, we observed a different expression pattern of PAI-2 protein in the epithelium of the cornea compared to conjunctiva and hypothesized a particular role of this inhibitor in regulating cell proliferation and turnover. We suggested that PAI-2 and the retinoblastoma related protein pRb2/p130 may cooperate with specific chromatin remodeling enzymes in modulating PAI-2 transcription, and investigated if transforming growth factor β-1 (TGF-β1) and phorbol 12-myristate 13-acetate (PMA) affect pRb2/p130 and PAI-2 interaction and/or their binding on PAI-2 promoter. We found that TGF-β1 or PMA treatments do not directly affect the interaction of PAI-2 and pRb2/p130 on the PAI-2 promoter. We hypothesize that, in corneal and conjunctival cells, TGF-β1 and PMA treatments indirectly control PAI-2 and pRb2/p130 levels inducing specific cellular signaling, via intracellular routes (MAPK/ERK, PKC) that may regulate the stability and the degradation of PAI-2 protein and/or PAI-2 mRNA.

Methods: : We determined the expression profile of a panel of genes related to the MAP Kinase (MAPK) signaling pathway including members of the MKKK, MKK, and MAPK families. The array included: activated transcription factor genes whose expression is induced by MAP Kinase signaling, Raf regulating proteins, MEKK1 interacting proteins, PAI-2 protein, pRb family proteins, scaffolding/anchoring proteins and cell cycle proteins regulated by the Erk1/2 pathway. The experiments have been performed in human cornea and conjunctiva primary cell lines, TGF-β1 and PMA treated or untreated, using a Human MAP Kinase Signaling Pathway PCR Array.

Results: : By comparing the gene expression profile of cornea and conjunctiva cell lines, we were able to identify differences and similarities in the expression pattern of a set of genes related to MAPK signaling. Our preliminary results showed that a variety of genes have differential expression in our experimental cell lines suggesting that the expression may be cell-type specific.

Keywords: cornea: epithelium • conjunctiva • anterior segment 
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