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Keratinocyte growth factor‐1 expression in healthy and diseased human periodontal tissues
Author(s) -
Li Min,
Firth James D.,
Putnins Edward E.
Publication year - 2005
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 - 10.1111/j.1600-0765.2004.00780.x
Subject(s) - keratinocyte growth factor , junctional epithelium , epithelium , biology , laser capture microdissection , connective tissue , keratinocyte , growth factor , fgf10 , cancer research , medicine , gene expression , fibroblast growth factor , cell culture , receptor , gene , biochemistry , genetics
Objectives: Keratinocyte growth factor‐1 (KGF‐1) is up‐regulated in chronic inflammation and specifically stimulates epithelial cell proliferation by signaling through the epithelial‐specific keratinocyte growth factor receptor (KGFR). We examined KGF‐1 and KGFR protein and gene expression in healthy and diseased periodontal tissues. Methods: Tissues were collected from patients with periodontal health or disease, immediately frozen and stained for KGF‐1 and KGFR protein expression. Laser capture microdissection of epithelial and connective tissue cells with reverse transcription–polymerase chain reaction (RT–PCR) examined KGF‐1 and KGFR gene expression profiles and enzymatic digestion with heparitinase, chondroitinase ABC or pre‐treatment with suramin examined epithelial surface molecule interactions with KGF‐1. Results: In tissues collected from healthy patients, KGF‐1 protein localized to areas of junctional and basal oral epithelial cells and was significantly increased in periodontal pocket epithelium ( p < 0.01) and in the oral epithelium ( p < 0.05) of disease‐associated tissues. KGFR localized to the junctional and the parabasal cells of oral epithelium, with the relative staining intensity being increased in disease‐associated pocket epithelium ( p < 0.05). Laser capture microdissection with RT–PCR confirmed KGF‐1 and KGFR were specifically expressed by connective tissue and epithelium, respectively. KGF‐1 localization to epithelial cells was largely eliminated by suramin pre‐treatment, indicating interaction with the KGFR. Conclusions: KGF‐1 and KGFR proteins are expressed in healthy periodontal tissues but significantly increased in diseased periodontal tissues. We hypothesize up‐regulation of KGF‐1 and KGFR protein associated with disease regulates epithelial cell behavior associated with onset and progression of periodontal pocket formation.