{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,19]],"date-time":"2025-10-19T15:31:28Z","timestamp":1760887888561},"reference-count":53,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2006,6,26]],"date-time":"2006-06-26T00:00:00Z","timestamp":1151280000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Periodontal Research"],"published-print":{"date-parts":[[2006,8]]},"abstract":"<jats:p><jats:bold>Background and Objective:\u2002<\/jats:bold> Regulation of epithelial cell behavior associated with periodontitis is not well elucidated but many responses will ultimately be regulated by growth factor receptors. Using a rat experimental periodontitis model, protein and gene expression of select growth factor receptors in junctional and pocket epithelium were examined.<\/jats:p><jats:p><jats:bold>Material and Methods:\u2002<\/jats:bold> Periodontal disease was induced by daily topical application of lipopolysaccharide using an established protocol. Animals were killed at time 0 (control), and at 2 and 8\u2003wk. Frozen tissue samples were collected from the right palatal gingival soft tissue, and the left periodontal tissues were decalcified and embedded in paraffin. Laser microdissection and quantitative reverse transcription\u2013polymerase chain reaction (qRT\u2013PCR) was used to quantify keratinocyte growth factor receptor (KGFR), hepatocyte growth factor receptor (HGFR), epidermal growth factor receptor (EGFR) and fibroblast growth factor receptor 1 (FGFR1) gene expression, and <jats:italic>in situ<\/jats:italic> RT\u2013PCR localized these increases to specific epithelial cells. Receptor protein expression was examined immunohistochemically. In cell culture, induction of HGFR and KGFR protein expression by serum, lipopolysaccharide and pro\u2010inflammatory cytokines were examined using flow cytometry.<\/jats:p><jats:p><jats:bold>Results:\u2002<\/jats:bold> Eight\u2010week tissue samples exhibited histological changes consistent with periodontitis. KGFR and HGFR gene and protein expression were significantly induced at the 8\u2003wk time point. KGFR expression was significantly up\u2010regulated in basal and parabasal pocket epithelial cells, but HGFR was up\u2010regulated throughout the pocket epithelium. In cell culture serum, lipopolysaccharide and pro\u2010inflammatory cytokines, interleukin\u20101\u03b2 and tumour necrosis factor\u2010\u03b1 significantly induced KGFR protein receptor expression, but HGFR expression was only induced by serum.<\/jats:p><jats:p><jats:bold>Conclusion:\u2002<\/jats:bold> KGFR and HGFR are highly up\u2010regulated in this model of periodontal disease and may play a significant role in regulating the proliferation and migration of pocket epithelium.<\/jats:p>","DOI":"10.1111\/j.1600-0765.2006.00881.x","type":"journal-article","created":{"date-parts":[[2006,6,26]],"date-time":"2006-06-26T07:58:27Z","timestamp":1151308707000},"page":"340-349","source":"Crossref","is-referenced-by-count":12,"title":["Regulation of epithelial cell growth factor receptor protein and gene expression using a rat periodontitis model"],"prefix":"10.1111","volume":"41","author":[{"given":"D.","family":"Ekuni","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J. 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