Abstract
Background and Objective: 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. Material and Methods: 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 wk. 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-polymerase chain reaction (qRT-PCR) 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 in situ RT-PCR 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-inflammatory cytokines were examined using flow cytometry. Results: Eight-week tissue samples exhibited histological changes consistent with periodontitis. KGFR and HGFR gene and protein expression were significantly induced at the 8 wk time point. KGFR expression was significantly up-regulated in basal and parabasal pocket epithelial cells, but HGFR was up-regulated throughout the pocket epithelium. In cell culture serum, lipopolysaccharide and pro-inflammatory cytokines, interleukin-1β and tumour necrosis factor-α significantly induced KGFR protein receptor expression, but HGFR expression was only induced by serum. Conclusion: KGFR and HGFR are highly up-regulated in this model of periodontal disease and may play a significant role in regulating the proliferation and migration of pocket epithelium.
| Original language | English |
|---|---|
| Pages (from-to) | 340-349 |
| Number of pages | 10 |
| Journal | Journal of Periodontal Research |
| Volume | 41 |
| Issue number | 4 |
| DOIs | |
| Publication status | Published - Aug 2006 |
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Keywords
- Hepatocyte growth factor receptor
- Keratinocyte growth factor receptor
- Laser dissection
- Periodontal disease
ASJC Scopus subject areas
- Dentistry(all)
Cite this
Regulation of epithelial cell growth factor receptor protein and gene expression using a rat periodontitis model. / Ekuni, Daisuke; Firth, J. D.; Putnins, E. E.
In: Journal of Periodontal Research, Vol. 41, No. 4, 08.2006, p. 340-349.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Regulation of epithelial cell growth factor receptor protein and gene expression using a rat periodontitis model
AU - Ekuni, Daisuke
AU - Firth, J. D.
AU - Putnins, E. E.
PY - 2006/8
Y1 - 2006/8
N2 - Background and Objective: 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. Material and Methods: 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 wk. 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-polymerase chain reaction (qRT-PCR) 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 in situ RT-PCR 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-inflammatory cytokines were examined using flow cytometry. Results: Eight-week tissue samples exhibited histological changes consistent with periodontitis. KGFR and HGFR gene and protein expression were significantly induced at the 8 wk time point. KGFR expression was significantly up-regulated in basal and parabasal pocket epithelial cells, but HGFR was up-regulated throughout the pocket epithelium. In cell culture serum, lipopolysaccharide and pro-inflammatory cytokines, interleukin-1β and tumour necrosis factor-α significantly induced KGFR protein receptor expression, but HGFR expression was only induced by serum. Conclusion: KGFR and HGFR are highly up-regulated in this model of periodontal disease and may play a significant role in regulating the proliferation and migration of pocket epithelium.
AB - Background and Objective: 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. Material and Methods: 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 wk. 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-polymerase chain reaction (qRT-PCR) 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 in situ RT-PCR 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-inflammatory cytokines were examined using flow cytometry. Results: Eight-week tissue samples exhibited histological changes consistent with periodontitis. KGFR and HGFR gene and protein expression were significantly induced at the 8 wk time point. KGFR expression was significantly up-regulated in basal and parabasal pocket epithelial cells, but HGFR was up-regulated throughout the pocket epithelium. In cell culture serum, lipopolysaccharide and pro-inflammatory cytokines, interleukin-1β and tumour necrosis factor-α significantly induced KGFR protein receptor expression, but HGFR expression was only induced by serum. Conclusion: KGFR and HGFR are highly up-regulated in this model of periodontal disease and may play a significant role in regulating the proliferation and migration of pocket epithelium.
KW - Hepatocyte growth factor receptor
KW - Keratinocyte growth factor receptor
KW - Laser dissection
KW - Periodontal disease
UR - http://www.scopus.com/inward/record.url?scp=33748527526&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=33748527526&partnerID=8YFLogxK
U2 - 10.1111/j.1600-0765.2006.00881.x
DO - 10.1111/j.1600-0765.2006.00881.x
M3 - Article
C2 - 16827730
AN - SCOPUS:33748527526
VL - 41
SP - 340
EP - 349
JO - Journal of Periodontal Research
JF - Journal of Periodontal Research
SN - 0022-3484
IS - 4
ER -