Hypoxia Augments Lipopolysaccharide-Induced Cytokine Expression in Periodontal Ligament Cells

Cao, Jian; Li, Chenjun; Ren, Yu; He, Yueqiu; Li, Yunming; Xu, Feng; Zhang, Gang; Tan, Yinghui

doi:10.1007/s10753-014-9865-6

Cited by 37 publications

(33 citation statements)

References 24 publications

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“…For instance, lack of TLR-2 and TLR-4 mediated responses in transplanted cardiomyocytes is predicted to increase their survival, albeit retaining their response to inflammatory cytokines in the infarcted heart [60]. Similarly, in vitro studies have shown that hypoxia enhances the LPS-induced inflammatory cytokine expression in human periodontal ligament cells [61, 62]. Hence, the predominantly nonresponsive behaviour of hESC-MSCs to bacterial challenge found in this study could be advantageous for their survival and probably in the longer term for optimal tissue regeneration.…”

Section: Discussionmentioning

confidence: 99%

Innate Immune Response of Human Embryonic Stem Cell‐Derived Fibroblasts and Mesenchymal Stem Cells to Periodontopathogens

Sriram

Natu

Islam

et al. 2016

Stem Cells International

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Periodontitis involves complex interplay of bacteria and host immune response resulting in destruction of supporting tissues of the tooth. Toll-like receptors (TLRs) play a role in recognizing microbial pathogens and eliciting an innate immune response. Recently, the potential application of multipotent stem cells and pluripotent stem cells including human embryonic stem cells (hESCs) in periodontal regenerative therapy has been proposed. However, little is known about the impact of periodontopathogens on hESC-derived progenies. This study investigates the effects of heat-killed periodontopathogens, namely, Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans, on TLR and cytokine expression profile of hESC-derived progenies, namely, fibroblasts (hESC-Fib) and mesenchymal stem cells (hESC-MSCs). Additionally, the serotype-dependent effect of A. actinomycetemcomitans on hESC-derived progenies was explored. Both hESC-Fib and hESC-MSCs constitutively expressed TLR-2 and TLR-4. hESC-Fib upon exposure to periodontopathogens displayed upregulation of TLRs and release of cytokines (IL-1β, IL-6, and IL-8). In contrast, hESC-MSCs were largely nonresponsive to bacterial challenge, especially in terms of cytokine production. Further, exposure of hESC-Fib to A. actinomycetemcomitans serotype c was associated with higher IL-8 production than serotype b. In contrast, the hESC-MSCs displayed no serotype-dependent response. Differential response of the two hESC progenies implies a phenotype-dependent response to periodontopathogens and supports the concept of immunomodulatory properties of MSCs.

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Section: Discussionmentioning

confidence: 99%

Innate Immune Response of Human Embryonic Stem Cell‐Derived Fibroblasts and Mesenchymal Stem Cells to Periodontopathogens

Sriram

Natu

Islam

et al. 2016

Stem Cells International

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“…Many epidemiological studies reported that the incidence of periodontitis in residents living in areas with altitudes over 4000 meters was significantly higher than that in residents living at sea level (Jian et al, 2014). Animal experiments also revealed that hypoxia may induce severe periodontitis (Xiao et al, 2012;Terrizzi et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

Hypoxia enhances periodontal ligament stem cell proliferation via the MAPK signaling pathway

He¹,

Cao²,

Zhang³

et al. 2016

Genet. Mol. Res.

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ABSTRACT. There is high incidence of periodontal disease in highaltitude environments; hypoxia may influence the proliferation and clone-forming ability of periodontal ligament stem cells (PDLSCs). The MAPK signaling pathway is closely correlated with cell proliferation, differentiation, and apoptosis. Thus, we isolated and cultured PDLSCs under hypoxic conditions to clarify the impact of hypoxia on PDLSC proliferation and the underlying mechanism. PDLSCs were separated and purified by the limiting dilution method and identified by flow cytometry. PDLSCs were cultured under hypoxic or normoxic conditions to observe their cloning efficiency. PDLSC proliferation at different oxygen concentrations was evaluated by MTT assay. Expression of p38/MAPK and MAPK/ERK signaling pathway members was detected by western blotting. Inhibitors for p38/MAPK or ERK were applied to PDLSCs to observe their impacts on clone formation and proliferation. Isolated PDLSCs exhibited typical stem cell morphological characteristics, strong abilities of globular clone formation and proliferation, and upregulated expression of mesenchymal stem cell markers. Stem cell marker expression was not statistically different between PDLSCs cultured under hypoxia and normoxia (P > 0.05). The clone number in the hypoxia group was significantly higher than that in the control (P < 0.05). PDLSC proliferation under hypoxia was higher than that of the control (P < 0.001). p38 and ERK1/2 phosphorylation in hypoxic PDLSCs was markedly enhanced compared to that in the control (P < 0.05). Either P38/MAPK inhibitor or ERK inhibitor treatment reduced clone formation and proliferation. Therefore, hypoxia enhanced PDLSC clone formation and proliferation by activating the p38/MAPK and ERK/MAPK signaling pathways.

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“…These events ultimately lead to tooth loss. 4,5 Although several studies have focused on the inflammatory responses to periodontitis, the effect of thermal stress on the inflammatory responses in PDL cells is largely unknown.…”

Section: Resultsmentioning

confidence: 99%

“…[9][10][11] Lipopolysaccharide (LPS)-stimulated PDL cells produce not only pro-inflammatory cytokines (IL-1b, IL-6, and IL-8) but also bone remodelling mediators (receptor activator of nuclear factor-kappa B ligand [RANKL]). 4,5 Thus, it is possible that thermosensitive TRP channels may play a significant role in periodontitis.…”

Section: Resultsmentioning

confidence: 99%

Induction of IL-6 and IL-8 by activation of thermosensitive TRP channels in human PDL cells

Son¹,

Hong²,

Chang³

et al. 2015

Archives of Oral Biology

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Hypoxia Augments Lipopolysaccharide-Induced Cytokine Expression in Periodontal Ligament Cells

Cited by 37 publications

References 24 publications

Innate Immune Response of Human Embryonic Stem Cell‐Derived Fibroblasts and Mesenchymal Stem Cells to Periodontopathogens

Innate Immune Response of Human Embryonic Stem Cell‐Derived Fibroblasts and Mesenchymal Stem Cells to Periodontopathogens

Hypoxia enhances periodontal ligament stem cell proliferation via the MAPK signaling pathway

Induction of IL-6 and IL-8 by activation of thermosensitive TRP channels in human PDL cells

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