Adenosine regulates the IL-1β-induced cellular functions of human gingival fibroblasts

Murakami, Shinya; Hashikawa, Tomoko; Saho, Teruyuki; Takedachi, Masahide; Nozaki, Tomoyoshi; Shimabukuro, Yoshio; Okada, Hiroshi

doi:10.1093/intimm/13.12.1533

Cited by 40 publications

(48 citation statements)

References 37 publications

(55 reference statements)

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“…The A 1 R was shown to enhance leukocyte recruitment [6][7][8]10], phagocytosis [9], generation of reactive oxygen species and NO and cytokine production [7][8][9][31][32][33][34]. We have previously shown on PMCs and peritoneal leukocytes that A 1 R is up-regulated shortly after inoculation [13,14], and we now show that A 1 R is a potent promoter of inflammation in the peritoneum.…”

Section: Discussionmentioning

confidence: 67%

Regulation of adenosine system at the onset of peritonitis

Nakav

Naamani

Chaimovitz

et al. 2009

Nephrology Dialysis Transplantation

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Background. Adenosine, a potent regulator of inflammation, is produced under stressful conditions due to degradation of ATP/ADP by the ectoenzymes CD39 and CD73. Adenosine is rapidly degraded by adenosine deaminase (ADA) or phosphorylated in the cell by adenosine kinase (AK). From four known receptors to adenosine, A 1 (A 1 R) promotes inflammation by a G i -coupled receptor. We have previously shown that A 1 R is up-regulated in the first hours following bacterial inoculation. The aim of the current study is to characterize the inflammatory mediators that regulate adenosine-metabolizing enzymes and A 1 R at the onset of peritonitis. Methods. Peritonitis was induced in CD1 mice by intraperitoneal injection of Escherichia coli. TNFα and IL-6 levels were determined in peritoneal fluid by enzymelinked immunosorbent assay. Adenosine-metabolizing enzymes and the A 1 R mRNA or protein levels were analyzed by quantitative PCR or by Western blot analysis, respectively. Results. We found that CD39 and CD73 were up-regulated in response to bacterial stimuli (6-fold the basal levels), while AK and ADA mRNA levels were down-regulated. Cytokine production and leukocyte recruitment were enhanced (2.5-fold) by treatment with an A 1 R agonist (2-chloro-N 6 -cyclopentyladenosine, 0.1mg/kg) and reduced (2.5-3-fold) by the A 1 R antagonist (8-cyclopentyl-1, 3-dipropylxanthine, 1mg/kg). In contrast to lipopolysaccharide, IL-1, TNF and IFNγ, only low IL-6 levels (0.01 ng/ml), in the presence of its soluble IL-6R (sIL-6R), were found to promote A 1 R expression on mesothelial cells. In mice, administration of neutralizing antibody to IL-6R or soluble gp130-Fc (sgp130-Fc) blocked peritoneal A 1 R up-regulation following inoculation. Conclusion. Bacterial products induce the production of adenosine by up-regulation of CD39 and CD73. Low IL-6-sIL-6R up-regulates the A 1 R to promote efficient inflammatory response against invading microorganisms.

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Section: Discussionmentioning

confidence: 67%

Regulation of adenosine system at the onset of peritonitis

Nakav

Naamani

Chaimovitz

et al. 2009

Nephrology Dialysis Transplantation

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“…Human PDL (HPDL) cells, dental pulp (HDP) cells, gingival fibroblasts (HGFs), and gingival epithelial cells (HGEs) were cultured according to previously described methods (Murakami et al, 2001(Murakami et al, , 2002Shimabukuro et al, 2005Shimabukuro et al, , 2009). We previously established a mouse PDL cell line, MPDL22, and used this as described in our earlier publication (Yamada et al, 2007).…”

Section: Cell Culture and Induction Of Pdl Cell Cytodifferentiationmentioning

confidence: 99%

Characterization of a Novel Periodontal Ligament-specific Periostin Isoform

et al. 2014

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Periostin is a mesenchymal cell marker predominantly expressed in collagen-rich fibrous connective tissues, including heart valves, tendons, perichondrium, periosteum, and periodontal ligament (PDL). Knockdown of periostin expression in mice results in early-onset periodontitis and failure of cardiac healing after acute myocardial infarction, suggesting that periostin is essential for connective tissue homeostasis and regeneration. However, its role(s) in periodontal tissues has not yet been fully defined. In this study, we describe a novel human isoform of periostin (PDL-POSTN). Isoform-specific analysis by reversetranscription polymerase chain-reaction (RT-PCR) revealed that PDL-POSTN was predominantly expressed in the PDL, with much lower expression in other tissues and organs. A PDL cell line transfected with PDL-POSTN showed enhanced alkaline phosphatase (ALPase) activity and calcified nodule formation, compared with cells transfected with the full-length periostin isoform. A neutralizing antibody against integrin-αv inhibited both ALPase activity and calcified nodule formation in cells transfected with PDL-POSTN. Furthermore, co-immunoprecipitation assays revealed that PDL-POSTN bound to integrin αvβ3 more strongly than the common isoform of periostin, resulting in strong activation of the integrin αvβ3-focal adhesion kinase (FAK) signaling pathway. These results suggest that PDL-POSTN positively regulates cytodifferentiation and mineralization in PDL cells through integrin αvβ3.

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“…The precipitated RNA was resuspended in 0.1% diethylpyrocarbonate-treated distilled water. cDNA was synthesized and amplified via PCR as described previously (Murakami et al, 2001). Oligonucleotide PCR primers specific for hyaluronan synthase (HAS) 1, 2, 3, and HPRT mRNA were synthesized by Clontech (Palo Alto, CA, USA).…”

Section: Detection Of Hyaluronan Synthase 1-3 (Has1 Has2 and Has3) mentioning

confidence: 99%

“…Among the extracellular matrices, hyaluronan (HA) plays multi-functional roles in the growth and differentiation of cells during the course of inflammatory reactions and the process of wound-healing and regeneration in periodontal tissues (Shimabukuro et al, 2005). We previously reported that adenosine enhanced HAS mRNA expression in HGF, and that the expression was markedly abrogated by the AdoR antagonist XAC (Murakami et al, 2001). This also indicates that intracellular signaling via AdoR can be monitored by HAS mRNA expression in gingival fibroblasts.…”

Section: Regulation Of Has 1 Mrna Expression By Ecto-adenosine Deaminasementioning

confidence: 99%

Activation of Adenosine Receptor on Gingival Fibroblasts

et al. 2006

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CD73 (ecto-5′-nucleotidase) on human gingival fibroblasts plays a role in the regulation of intracellular cAMP levels through the generation of adenosine, which subsequently activates adenosine receptors. In this study, we examined the involvement of ecto-adenosine deaminase, which can be anchored to CD26 on human gingival fibroblasts, in metabolizing adenosine generated by CD73, and thus attenuating adenosine receptor activation. Ecto-adenosine deaminase expression on fibroblasts could be increased by pre-treatment with a lysate of Jurkat cells, a cell line rich in cytoplasmic adenosine deaminase. Interestingly, the cAMP response to adenosine generated from 5′-AMP via CD73 and the ability of 5′-AMP to induce hyaluronan synthase 1 mRNA were significantly decreased by the pre-treatment of fibroblasts with Jurkat cell lysate. This inhibitory effect was reversed by the specific adenosine deaminase inhibitor. These results suggest that ectoadenosine deaminase metabolizes CD73-generated adenosine and regulates adenosine receptor activation.

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Adenosine regulates the IL-1β-induced cellular functions of human gingival fibroblasts

Cited by 40 publications

References 37 publications

Regulation of adenosine system at the onset of peritonitis

Regulation of adenosine system at the onset of peritonitis

Characterization of a Novel Periodontal Ligament-specific Periostin Isoform

Activation of Adenosine Receptor on Gingival Fibroblasts

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