Elevation of galectin-9 as an inflammatory response in the periodontal ligament cells exposed to Porphylomonas gingivalis lipopolysaccharide in vitro and in vivo

Kasamatsu, Atsushi; Uzawa, Katsuhiro; Shimada, Ken; Shiiba, Masashi; Otsuka, Yoko; Seki, Naohiko; Abiko, Yoshimitsu; Tanzawa, Hideki

doi:10.1016/j.biocel.2004.07.014

Cited by 42 publications

(37 citation statements)

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“…1). This is in line with the observations made in IFN-γ-stimulated cultured human endothelial cells, fibroblasts, monocytes, and macrophages [32][33][34], while …”

Section: Discussionsupporting

confidence: 91%

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Proinflammatory stimuli induce galectin‐9 in human mesenchymal stromal cells to suppress T‐cell proliferation

et al. 2013

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Human multipotent mesenchymal stromal cells (MSCs) are clinically applied to treat autoimmune diseases and graft-versus-host disease due to their immunomodulatory properties. Several molecules have been identified to mediate these effects, including constitutively expressed galectin-1. However, there are indications in the literature that MSCs exert enhanced immunosuppressive functions after interaction with an inflammatory environment. Therefore, we analyzed how inflammatory stimuli influence the expression of the galectin network in MSCs and functionally tested the relevance for the immunomodulatory effects of MSCs. We found that galectin-9 was strongly induced in MSCs upon interaction with activated PBMCs. Proinflammatory cytokines, such as interferon-gamma (IFN-γ) and tumor necrosis factor-alpha (TNF-α), and also ligands of the Toll-like receptors (TLRs) TLR2, TLR3, and TLR4 elicited similar induction of galectin-9 in activated PBMCs. Galectin-9 was not only upregulated intracellularly, but also released by MSCs in significant amounts into the supernatant after exposure to proinflammatory stimuli. In proliferation assays, MSCs with a galectin-9 knockdown lost a significant portion of their antiproliferative effects on T cells. In conclusion, we found that unlike constitutively expressed galectin-1, galectin-9 is induced by several proinflammatory stimuli and released by MSCs. Thus, galectin-9 contributes to the inducible immunomodulatory functions of MSCs.Keywords: Galectin-9 r Immunosuppressive effects r Mesenchymal stromal cells r Proinflammatory stimuli r T-cell proliferation IntroductionHuman multipotent mesenchymal stromal cells (MSCs) possess immunomodulatory properties. In addition, MSCs migrate to sites Correspondence: Dr. Friederike Gieseke e-mail: gieseke@kinderkrebs-forschung.de of tissue injury or inflammation, where they participate in wound healing [1]. Initially, MSCs were thought to mediate tissue repair because of their differentiation potential. However, it has become more evident that the production of soluble factors is the critical step for tissue repair [2]. In addition, BM-derived MSCs, which are immunosuppressive in vitro and in vivo [3], use soluble factors to mediate these effects at least in vitro [4] Eur. J. Immunol. 2013. 43: 2741-2749 interest for treatment of immune-mediated diseases. In particular, promising results of i.v. infusion of MSCs for treatment of steroid refractory graft-versus-host disease (GvHD) have been observed [5][6][7]. Several soluble molecules are involved in immune suppression mediated by human MSCs, such as prostaglandin E2 (PGE2) [8], indoleamine-2,3-dioxygenase (IDO) [9], heme oxygenase-1 [10], human leukocyte antigen G (HLA-G5) [11], and galectin-1 [12], among others. Furthermore, it was shown that interactions between inflammatory cells and MSCs induce or activate the immunosuppressive properties of MSCs; in this process, interferon-gamma (IFN-γ) appeared to be the most important cytokine [9,13,14].In the present study, we focused on the role of gale...

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“…1). This is in line with the observations made in IFN-γ-stimulated cultured human endothelial cells, fibroblasts, monocytes, and macrophages [32][33][34], while …”

Section: Discussionsupporting

confidence: 91%

“…Additionally, Gal-9 increase was observed in the presence of TLR ligands, LPS, and doublestranded RNA [34,36]. Thus, there is evidence that Gal-9 expression can be upregulated by inflammatory cytokines and bacterial components caused by infections [28].…”

Section: T Cells and (B) Cd8mentioning

confidence: 98%

Proinflammatory stimuli induce galectin‐9 in human mesenchymal stromal cells to suppress T‐cell proliferation

et al. 2013

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“…5). This is consistent with previous results showing that galectin-9 expression was elevated by LPS in human periodontal ligament cells and monocytic THP-1 cells [12,30]. However, unlike in the spleen, RuGlec9 mRNA expression in the liver was not significantly affected by 10 mg/ml LPS (data not shown).…”

Section: Induction Of Ruglec9 Mrna Expression By Lpssupporting

confidence: 93%

Molecular characterization of a tandem-repeat galectin-9 (RuGlec9) from Korean rose bitterling (Rhodeus uyekii)

Kong

Kim

et al. 2012

Fish & Shellfish Immunology

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“…Total RNA was isolated from cells using TRIzol reagent (Invitrogen, Carlsbad, CA), and reverse transcribed using Ready-to-Go You-Prime first-strand beads (Amersham Biosciences, Little Chalfont, Buckinghamshire, UK) and oligo (dT) primer (Sigma Genosys, Ishikari, Japan) (24). qRT-PCR was performed to evaluate the expression level of HDAC6 mRNA in the nine OSCC-derived cell lines, NOKs, tumors, and paired normal oral tissues from 50 patients with OSCC using a LightCycler FastStart DNA Master SYBR Green I kit (Roche Diagnostics GmbH, Mannheim, Germany), according to the procedure described by the manufacturer.…”

Section: Cellsmentioning

confidence: 99%

Aberrant expression of histone deacetylase 6 in oral squamous cell carcinoma

Sakuma

Uzawa²,

Onda³

et al. 2006

Int J Oncol

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116

122

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Abstract.The structure and function of chromatin can be altered by modifications to histone. Histone acetylation is a reversible process governed by histone acetyltransferases and histone deacetylases (HDACs). HDAC6 is a subtype of the HDAC family that deacetylates ·-tubulin and increases cell motility. We investigated the expression levels of HDAC6 mRNA and protein expression in oral squamous cell carcinoma (OSCC)-derived cell lines and human primary OSCCs to elucidate the potential involvement of HDAC6 in OSCC. Using quantitative real-time reverse transcription polymerase chain reaction and Western blots on nine OSCC-derived cell lines and normal oral keratinocytes (NOKs), HDAC6 mRNA and protein expression were commonly up-regulated in all cell lines compared with the NOKs. Immunofluorescence analysis detected HDAC6 protein in the cytoplasm of OSCC cell lines. Similar to OSCC cell lines, high frequencies of HDAC6 up-regulation were evident in both mRNA (74%) and protein (51%) levels of primary tumors. Among the clinical variables analyzed, the clinical tumor stage was found to be associated with the HDAC6 expression states. The analysis indicated a significant difference in the HDAC6 expression level between the early stage (stage I and II) and advancedstage (stage III and IV) tumors (P=0.014). These results suggest that HDAC6 expression may be correlated with tumor aggressiveness and offer clues to the planning of new treatments.

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Elevation of galectin-9 as an inflammatory response in the periodontal ligament cells exposed to Porphylomonas gingivalis lipopolysaccharide in vitro and in vivo

Cited by 42 publications

References 50 publications

Proinflammatory stimuli induce galectin‐9 in human mesenchymal stromal cells to suppress T‐cell proliferation

Proinflammatory stimuli induce galectin‐9 in human mesenchymal stromal cells to suppress T‐cell proliferation

Molecular characterization of a tandem-repeat galectin-9 (RuGlec9) from Korean rose bitterling (Rhodeus uyekii)

Aberrant expression of histone deacetylase 6 in oral squamous cell carcinoma

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