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- Publisher Website: 10.1034/j.1600-0765.2002.01007.x
- Scopus: eid_2-s2.0-0036885831
- PMID: 12472839
- WOS: WOS:000180119600007
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Article: Treponema denticola may stimulate both epithelial proliferation and apoptosis through MAP kinase signal pathways
Title | Treponema denticola may stimulate both epithelial proliferation and apoptosis through MAP kinase signal pathways |
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Authors | |
Keywords | Cell Signaling Mitogenactivated Protein Kinase Periodontal Diseases Treponema Denticola, Epithelial Proliferation, Apoptosis |
Issue Date | 2002 |
Publisher | Wiley-Blackwell Publishing, Inc.. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0022-3484&site=1 |
Citation | Journal of Periodontal Research, 2002, v. 37 n. 6, p. 445-455 How to Cite? |
Abstract | Mitogen-activated protein kinases (MAP kinases) play a key role in the regulation of cell survival and death. Effects of Treponema denticola ATCC 35405 on ERK, p38 and JNK MAP kinases, and cell behavior was studied using non-keratinizing periodontal ligament epithelial cells (PLE) in vitro. Compared to Chinese hamster ovary cells, human cervix adenocarcinoma cells, human osteosacroma cells and human gingival fibroblasts, PLE cells were much more resistant to T. denticola-induced reduction in cell viability, assayed by tetrazolium and crystal Violet assays. A low dose of 5 × 10 7 T. denticola cells/ml increased DNA synthesis ([ 3H]thymidine uptake) in PLE cells but at higher concentrations DNA synthesis was decreased. TUNEL staining analysis showed that about 50% of epithelial cells in onolayers died through apoptosis when exposed to a high dose of 10 11 T. denticola/ml for 24 h. Morphological light and electron microscopic analysis supported the idea that both apoptotic and necrotic cell death took place. Rounding, membrane damage, fragmentation and detachment were observed in selective cells of both mono- and multilayered PLE cultures challenged with T. denticola. Western blot analysis using MAP kinase phosphospecific antibodies showed that T. denticola strongly but transiently activated ERK1 and ERK2, signals mediating cell proliferation, and JNK and p38. kinases mediating apoptosis. While a specific inhibitor of the ERK MAP kinase pathway prevented the T. denticola stimulation of cell proliferation, inhibitor of p38 increased the cell numbers in T. denticola-treated cultures. The results suggest that T. denticola activates epithelial cell MAP kinase signal pathways controlling cell proliferation and cell survival. In addition, T. denticola exerts cytotoxic effects that appear to predominate at higher bacterial concentrations. © Blackwell Munksgaard, 2002. |
Persistent Identifier | http://hdl.handle.net/10722/154216 |
ISSN | 2023 Impact Factor: 3.4 2023 SCImago Journal Rankings: 0.895 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Leung, WK | en_US |
dc.contributor.author | Wu, Q | en_US |
dc.contributor.author | Hannam, PM | en_US |
dc.contributor.author | Mcbride, BC | en_US |
dc.contributor.author | Uitto, VJ | en_US |
dc.date.accessioned | 2012-08-08T08:23:56Z | - |
dc.date.available | 2012-08-08T08:23:56Z | - |
dc.date.issued | 2002 | en_US |
dc.identifier.citation | Journal of Periodontal Research, 2002, v. 37 n. 6, p. 445-455 | en_US |
dc.identifier.issn | 0022-3484 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/154216 | - |
dc.description.abstract | Mitogen-activated protein kinases (MAP kinases) play a key role in the regulation of cell survival and death. Effects of Treponema denticola ATCC 35405 on ERK, p38 and JNK MAP kinases, and cell behavior was studied using non-keratinizing periodontal ligament epithelial cells (PLE) in vitro. Compared to Chinese hamster ovary cells, human cervix adenocarcinoma cells, human osteosacroma cells and human gingival fibroblasts, PLE cells were much more resistant to T. denticola-induced reduction in cell viability, assayed by tetrazolium and crystal Violet assays. A low dose of 5 × 10 7 T. denticola cells/ml increased DNA synthesis ([ 3H]thymidine uptake) in PLE cells but at higher concentrations DNA synthesis was decreased. TUNEL staining analysis showed that about 50% of epithelial cells in onolayers died through apoptosis when exposed to a high dose of 10 11 T. denticola/ml for 24 h. Morphological light and electron microscopic analysis supported the idea that both apoptotic and necrotic cell death took place. Rounding, membrane damage, fragmentation and detachment were observed in selective cells of both mono- and multilayered PLE cultures challenged with T. denticola. Western blot analysis using MAP kinase phosphospecific antibodies showed that T. denticola strongly but transiently activated ERK1 and ERK2, signals mediating cell proliferation, and JNK and p38. kinases mediating apoptosis. While a specific inhibitor of the ERK MAP kinase pathway prevented the T. denticola stimulation of cell proliferation, inhibitor of p38 increased the cell numbers in T. denticola-treated cultures. The results suggest that T. denticola activates epithelial cell MAP kinase signal pathways controlling cell proliferation and cell survival. In addition, T. denticola exerts cytotoxic effects that appear to predominate at higher bacterial concentrations. © Blackwell Munksgaard, 2002. | en_US |
dc.language | eng | en_US |
dc.publisher | Wiley-Blackwell Publishing, Inc.. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0022-3484&site=1 | en_US |
dc.relation.ispartof | Journal of Periodontal Research | en_US |
dc.subject | Cell Signaling | en_US |
dc.subject | Mitogenactivated Protein Kinase | en_US |
dc.subject | Periodontal Diseases | en_US |
dc.subject | Treponema Denticola, Epithelial Proliferation, Apoptosis | en_US |
dc.title | Treponema denticola may stimulate both epithelial proliferation and apoptosis through MAP kinase signal pathways | en_US |
dc.type | Article | en_US |
dc.identifier.email | Leung, WK: ewkleung@hkucc.hku.hk | en_US |
dc.identifier.authority | Leung, WK=rp00019 | en_US |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.doi | 10.1034/j.1600-0765.2002.01007.x | - |
dc.identifier.pmid | 12472839 | - |
dc.identifier.scopus | eid_2-s2.0-0036885831 | en_US |
dc.identifier.hkuros | 80749 | - |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-0036885831&selection=ref&src=s&origin=recordpage | en_US |
dc.identifier.volume | 37 | en_US |
dc.identifier.issue | 6 | en_US |
dc.identifier.spage | 445 | en_US |
dc.identifier.epage | 455 | en_US |
dc.identifier.isi | WOS:000180119600007 | - |
dc.publisher.place | United States | en_US |
dc.identifier.scopusauthorid | Leung, WK=25224691800 | en_US |
dc.identifier.scopusauthorid | Wu, Q=55188342800 | en_US |
dc.identifier.scopusauthorid | Hannam, PM=6602614873 | en_US |
dc.identifier.scopusauthorid | McBride, BC=7102465580 | en_US |
dc.identifier.scopusauthorid | Uitto, VJ=7004455896 | en_US |
dc.identifier.issnl | 0022-3484 | - |