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Conference Paper: Calcium signal facilitates the immediate induction of HIF-1α by lipopolysaccharide

TitleCalcium signal facilitates the immediate induction of HIF-1α by lipopolysaccharide
Authors
KeywordsPeriodontics
Cell biology
Periodontium-gingiva
Periodontal disease
Host-microbial interactions
Issue Date2010
PublisherSage Publications, Inc. The Journal's web site is located at http://jdr.sagepub.com/
Citation
The 24th IADR-SEA Division Annual Scientific Meeting, Taipei, Taiwan, 19-21 September 2010. In Journal of Dental Research, 2010, v. 89 n. Spec Iss C, p. Abstract no. 130 How to Cite?
AbstractObjectives: hypoxia-inducible factor 1 alpha (HIF-1α) is an oxygen-sensitive nuclear transcription factor, which responds to hypoxia or non-hypoxia stimuli by transcribing dozens of downstream genes and participates profoundly in cellular physiology. The regulation of HIF-1α is typically through oxygen-sensitive prolyl hydroxylases (PHDs), which hydroxylize HIF-1α to facilitate its degradation. Other mechanisms include the regulation of the transcription and translation of HIF-1α. We previously reported that lipopolysaccharide (LPS) induces HIF-1α in human primary gingival fibroblasts (HGF). The present study aimed to explore the underlying mechanism via looking into Ca2+/Calmodulin-dependent protein kinase II (CaMKII) and calcineurin pathway. Methods: Human gingival biopsies were harvested from teeth scheduled for extraction because of orthodontic reasons. HGFs were cultured and subjected to LPS treatment only or in combination with actinomycin D (transcription inhibitor), dimethyloxalylglycine (DMOG, PHDs inhibitor), KN-93 (CaMKII inhibitor) or cyclosporin A (calcineurin inhibitor). Realtime RT-PCR, immunoprecipitation and western blotting were performed to detect the transcript and peptide of HIF-1α. Results: Although HIF-1α accumulation could be detected as early as 3 hours after LPS challenge, the transcription level of HIF-1α gene did not increase until after 6 hours. Moreover, when transcription was prohibited by actinomycin D, LPS still induced HIF-1α. Similarly, LPS enhanced the HIF-1α accumulation in DMOG-treated cells, indicating that the LPS effect on HIF-1α may not be through actions of PHDs. However, cyclosporin A and KN-93 dramatically attenuated the LPS-induced HIF-1α accumulation. Conclusions: Ca2+-CaMKII-calcineurin pathway may be essential to the immediate accumulation of HIF-1α in HGFs as a response to LPS challenge.
Persistent Identifierhttp://hdl.handle.net/10722/140035
ISSN
2015 Impact Factor: 4.602
2015 SCImago Journal Rankings: 1.714

 

DC FieldValueLanguage
dc.contributor.authorLi, JP-
dc.contributor.authorFung, ML-
dc.contributor.authorLi, F-
dc.contributor.authorXu, A-
dc.contributor.authorLeung, WK-
dc.date.accessioned2011-09-23T06:05:11Z-
dc.date.available2011-09-23T06:05:11Z-
dc.date.issued2010-
dc.identifier.citationThe 24th IADR-SEA Division Annual Scientific Meeting, Taipei, Taiwan, 19-21 September 2010. In Journal of Dental Research, 2010, v. 89 n. Spec Iss C, p. Abstract no. 130-
dc.identifier.issn0022-0345-
dc.identifier.urihttp://hdl.handle.net/10722/140035-
dc.description.abstractObjectives: hypoxia-inducible factor 1 alpha (HIF-1α) is an oxygen-sensitive nuclear transcription factor, which responds to hypoxia or non-hypoxia stimuli by transcribing dozens of downstream genes and participates profoundly in cellular physiology. The regulation of HIF-1α is typically through oxygen-sensitive prolyl hydroxylases (PHDs), which hydroxylize HIF-1α to facilitate its degradation. Other mechanisms include the regulation of the transcription and translation of HIF-1α. We previously reported that lipopolysaccharide (LPS) induces HIF-1α in human primary gingival fibroblasts (HGF). The present study aimed to explore the underlying mechanism via looking into Ca2+/Calmodulin-dependent protein kinase II (CaMKII) and calcineurin pathway. Methods: Human gingival biopsies were harvested from teeth scheduled for extraction because of orthodontic reasons. HGFs were cultured and subjected to LPS treatment only or in combination with actinomycin D (transcription inhibitor), dimethyloxalylglycine (DMOG, PHDs inhibitor), KN-93 (CaMKII inhibitor) or cyclosporin A (calcineurin inhibitor). Realtime RT-PCR, immunoprecipitation and western blotting were performed to detect the transcript and peptide of HIF-1α. Results: Although HIF-1α accumulation could be detected as early as 3 hours after LPS challenge, the transcription level of HIF-1α gene did not increase until after 6 hours. Moreover, when transcription was prohibited by actinomycin D, LPS still induced HIF-1α. Similarly, LPS enhanced the HIF-1α accumulation in DMOG-treated cells, indicating that the LPS effect on HIF-1α may not be through actions of PHDs. However, cyclosporin A and KN-93 dramatically attenuated the LPS-induced HIF-1α accumulation. Conclusions: Ca2+-CaMKII-calcineurin pathway may be essential to the immediate accumulation of HIF-1α in HGFs as a response to LPS challenge.-
dc.languageeng-
dc.publisherSage Publications, Inc. The Journal's web site is located at http://jdr.sagepub.com/-
dc.relation.ispartofJournal of Dental Research-
dc.rightsJournal of Dental Research. Copyright © Sage Publications, Inc.-
dc.subjectPeriodontics-
dc.subjectCell biology-
dc.subjectPeriodontium-gingiva-
dc.subjectPeriodontal disease-
dc.subjectHost-microbial interactions-
dc.titleCalcium signal facilitates the immediate induction of HIF-1α by lipopolysaccharide-
dc.typeConference_Paper-
dc.identifier.emailFung, ML: fungml@hkucc.hku.hk-
dc.identifier.emailXu, A: amxu@hkucc.hku.hk-
dc.identifier.emailLeung, WK: ewkleung@hkucc.hku.hk-
dc.identifier.authorityFung, ML=rp00433-
dc.identifier.authorityXu, A=rp00485-
dc.identifier.authorityLeung, WK=rp00019-
dc.identifier.hkuros195770-
dc.identifier.hkuros181632-
dc.identifier.volume89-
dc.identifier.issueSpec Iss C-
dc.identifier.spageAbstract no. 130-
dc.identifier.epageAbstract no. 130-
dc.publisher.placeUnited States-
dc.description.otherThe 24th Annual Scientific Meeting of the International Association for Dental Research-SEA Division (IADR-SEA 2010) and the 21st Meeting of the South East Asia Association for Dental Education (SEAADE 2010), Taipei, Taiwan, 19-21 September 2010. In Journal of Dental Research, 2010, v. 89 n. Special Issue C, abstract no. 130 (SEA Division)-

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