Inflammation-associated lysyl oxidase protein expression in vivo, and modulation by FGF-2 plus IGF-1 |
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Authors: | P C Trackman Rudolph J Graham Howard K Bittner David L Carnes James A Gilles Dana T Graves |
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Institution: | (1) Division of Oral Biology, Boston University Medical Center, 700 Albany Street, W-201E, Boston, MA 02118, USA e-mail trackman@acs.bu.edu Tel. +1–617–638–4076; fax +1–617–638–4924, US;(2) Department of Biochemistry, Boston University School of Medicine, Boston, Mass., USA, US;(3) Department of Endodontics, University of Texas, Health Science Center, San Antonio, Tex., USA, US |
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Abstract: | Lysyl oxidase is the extracellular enzyme that catalyzes oxidative deamination of peptidyl-lysine residues in elastin precursors,
and lysine and hydroxylysine residues in collagen precursors to form peptidyl-aldehydes. These aldehydes then spontaneously
condense to crosslink collagen and elastin and thereby allow the formation of a mature and functional extracellular matrix.
In the present study, cryosections made from aseptic immune-induced periapical lesions experimentally generated in laboratory
rats were examined by immunohistochemistry to investigate whether lysyl oxidase protein expression is altered in inflamed
oral tissues. Periapical lesions are experimentally induced endodontic lesions of tooth roots. In addition, the effect of
administration of a mixture of fibroblast growth factor (FGF)-2 and insulin-like growth factor (IGF)-1 into these lesions
on lysyl oxidase expression was determined. Lysyl oxidase expression was found to be increased in non-mineralized connective
tissue adjacent to inflamed lesions. Morphometric analyses indicated that maximum lysyl oxidase expression occurred at a discrete
distance from the lesion not exceeding 350 μm from the inflammatory cells. Staining was associated with mesenchymal cells
with a fibroblastic morphology. No lysyl oxidase staining was found near teeth where no lesion was induced. Application of
a mixture of FGF-2 and IGF-1 resulted in a further twofold increase in lysyl oxidase expression. These results provide a new
in vivo model to study lysyl oxidase regulation, and suggest that inflammatory cells may control lysyl oxidase expression
in oral tissues, possibly by a mechanism involving secretion of cytokines and other factors, probably contributing to the
regulation of extracellular matrix accumulation.
Accepted: 19 December 1998 |
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