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Photoreactivation of ultraviolet radiation‐induced basic fibroblast growth factor (bFGF) and the role of bFGF in corneal lesion formation in Monodelphis domestica
Author(s) -
Ley Ronald D.,
Miska Katarzyna B.,
Kusewitt Donna F.
Publication year - 2001
Publication title -
environmental and molecular mutagenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1
H-Index - 87
eISSN - 1098-2280
pISSN - 0893-6692
DOI - 10.1002/em.1069
Subject(s) - basic fibroblast growth factor , biology , autocrine signalling , in situ hybridization , paracrine signalling , corneal epithelium , corneal neovascularization , cornea , immunohistochemistry , pyrimidine dimer , neovascularization , growth factor , angiogenesis , pathology , microbiology and biotechnology , immunology , cancer research , dna damage , gene expression , medicine , cell culture , genetics , receptor , dna , neuroscience , gene
Chronic ultraviolet radiation (UVR) exposure to the eyes of Monodelphis domestica causes corneal opacification, neovascularization, and fibrosarcoma induction. By immunohistochemistry and Western blotting, we have shown that one to four exposures of the eyes of this opossum to UVR enhances basic fibroblast growth factor (bFGF) expression by the corneal epithelium. Treatment with photoreactivating light, which selectively removes UVR‐induced pyrimidine dimers, suppresses bFGF induction, indicating that UVR induction of bFGF is ultimately due to DNA damage. Furthermore, UVR‐induced corneal tumors derived from corneal keratocytes express bFGF mRNA and protein, as determined by immunohistochemistry and in situ hybridization. Taken together, these findings suggest that bFGF acts in both an autocrine and a paracrine manner to stimulate corneal fibroplasia, neovascularization, and tumor development. Environ. Mol. Mutagen. 38:175–179, 2001 © 2001 Wiley‐Liss, Inc.