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Article: Treponema denticola may stimulate both epithelial proliferation and apoptosis through MAP kinase signal pathways

TitleTreponema denticola may stimulate both epithelial proliferation and apoptosis through MAP kinase signal pathways
Authors
KeywordsCell Signaling
Mitogenactivated Protein Kinase
Periodontal Diseases
Treponema Denticola, Epithelial Proliferation, Apoptosis
Issue Date2002
PublisherWiley-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?
AbstractMitogen-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 Identifierhttp://hdl.handle.net/10722/154216
ISSN
2015 Impact Factor: 2.474
2015 SCImago Journal Rankings: 0.932
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLeung, WKen_US
dc.contributor.authorWu, Qen_US
dc.contributor.authorHannam, PMen_US
dc.contributor.authorMcbride, BCen_US
dc.contributor.authorUitto, VJen_US
dc.date.accessioned2012-08-08T08:23:56Z-
dc.date.available2012-08-08T08:23:56Z-
dc.date.issued2002en_US
dc.identifier.citationJournal of Periodontal Research, 2002, v. 37 n. 6, p. 445-455en_US
dc.identifier.issn0022-3484en_US
dc.identifier.urihttp://hdl.handle.net/10722/154216-
dc.description.abstractMitogen-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.languageengen_US
dc.publisherWiley-Blackwell Publishing, Inc.. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0022-3484&site=1en_US
dc.relation.ispartofJournal of Periodontal Researchen_US
dc.subjectCell Signalingen_US
dc.subjectMitogenactivated Protein Kinaseen_US
dc.subjectPeriodontal Diseasesen_US
dc.subjectTreponema Denticola, Epithelial Proliferation, Apoptosisen_US
dc.titleTreponema denticola may stimulate both epithelial proliferation and apoptosis through MAP kinase signal pathwaysen_US
dc.typeArticleen_US
dc.identifier.emailLeung, WK: ewkleung@hkucc.hku.hken_US
dc.identifier.authorityLeung, WK=rp00019en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1034/j.1600-0765.2002.01007.x-
dc.identifier.pmid12472839-
dc.identifier.scopuseid_2-s2.0-0036885831en_US
dc.identifier.hkuros80749-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0036885831&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume37en_US
dc.identifier.issue6en_US
dc.identifier.spage445en_US
dc.identifier.epage455en_US
dc.identifier.isiWOS:000180119600007-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridLeung, WK=25224691800en_US
dc.identifier.scopusauthoridWu, Q=55188342800en_US
dc.identifier.scopusauthoridHannam, PM=6602614873en_US
dc.identifier.scopusauthoridMcBride, BC=7102465580en_US
dc.identifier.scopusauthoridUitto, VJ=7004455896en_US

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