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Keratinocyte growth factor (KGF)‐1 and ‐2 protein and gene expression in human gingival fibroblasts
Author(s) -
Sanaie AliReza,
Firth James D.,
Uitto VeliJukka,
Putnins Edward E.
Publication year - 2002
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1034/j.1600-0765.2002.90770a.x
Subject(s) - keratinocyte growth factor , proinflammatory cytokine , porphyromonas gingivalis , connective tissue , biology , cytokine , fgf10 , fibroblast growth factor , growth factor , microbiology and biotechnology , paracrine signalling , fibroblast , immunology , cell culture , inflammation , biochemistry , genetics , receptor , bacteria
The onset and progression of jreiodontal disease is associated with significant changes in the epithelial component of the attachment complex. From the early to the advanced stages of jreiodontal disease increased epithelial cell proliferation, migration and invasion into the surrounding connective tissue takes place. Concomitantly there is a significant increase in proinflammatory cytokine expression in jreiodontal tissue and quantitative and qualitative changes in the subgingival microflora, including an increase in gram‐negative microorganisms. One of the most significant virulence factors of these bacteria is lipopolysaccharide (LPS) connected to the outer membrane. Two important growth factors controlling epithelial behavior are Keratinocyte Growth Factor‐1 (KGF‐1) and ‐2 (KGF‐2). Connective tissue cells express these growth factors, but only epithelial cells respond to them. We studied the effect of proinflammatory cytokines and LPS on gingival fibroblast expression of KGF‐1 and KGF‐2 in vitro . Gingival fibroblasts were found to express KGF‐1 and ‐2 in culture but only KGF‐1 protein and gene expression was stimulated by serum, in a concentration‐dependent manner by proinflammatory cytokines IL‐1α, IL‐1β, TNF‐α and IL‐6 and LPS isolated from Porphyromonas gingivalis and Escherichia coli . The local increase in proinflammatory cytokine expression and the accumulation of LPS in disease sites may therefore stimulate gingival fibroblast expression of KGF‐1. We hypothesize that this local increase in KGF‐1 expression may, via a paracrine mechanism, stimulate local epithelial cell proliferation, migration and invasion during the onset and progression of jreiodontitis.

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