Nacksung Kim

Chonnam National University, Gwangju, Gwangju, South Korea

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Publications (71)407.86 Total impact

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    Jung Ha Kim · Kabsun Kim · Inyoung Kim · Semun Seong · Nacksung Kim ·
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    ABSTRACT: Negative regulator of reactive oxygen species (NRROS) is known to repress ROS generation in phagocytes. In this study, we examined the roles of NRROS in both osteoclasts and osteoblasts. Our results demonstrate that NRROS negatively regulates the differentiation of osteoclasts, but not osteoblasts. Further, overexpression of NRROS in osteoclast precursor cells attenuates RANKLinduced osteoclast differentiation. Conversely, osteoclast differentiation is enhanced upon siRNA-mediated knockdown of NRROS. Additionally, NRROS attenuates RANKLinduced NF-κB activation, as well as degradation of the NOX1 and NOX2 proteins, which are required for ROS generation. Based on our observations, we present NRROS as a novel negative regulator of RANKL-induced osteoclastogenesis.
    Moleculer Cells 10/2015; DOI:10.14348/molcells.2015.0177 · 2.09 Impact Factor
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    ABSTRACT: To investigate the role played by NKT cells in osteoclastogenesis and their effects on inflammatory bone destruction. Patients with RA (n=25) and healthy controls (n=12) were enrolled in this study. In vitro osteoclastogenesis experiments were performed using peripheral blood mononuclear cells (PBMCs) in the presence of M-CSF and receptor activator of nuclear factor κB ligand (RANKL). PBMCs were cultured in vitro with α-galactosylceramide (αGalCer), and proliferation indices of NKT cells were estimated by flow cytometry. In vivo effects of αGalCer-stimulated NKT cells on inflammation and bone destruction were determined in collagen-induced arthritis (CIA) mice. In vitro osteoclastogenesis was found to be significantly inhibited by αGalCer in healthy controls, but not in RA patients. Proliferative responses of NKT cells and STAT-1 phosphorylation in monocytes in response to αGalCer were impaired in RA patients. Notably, αGalCer-stimulated NKT cells inhibited osteoclastogenesis mainly via interferon-γ production, in a cytokine-dependent manner (not by cell-cell contact), and down-regulated osteoclast-associated genes. αGalCer-treated mice showed less severe arthritis and reduced bone destruction. Moreover, proinflammatory cytokine expression in arthritic joints was found to be reduced by αGalCer treatment. This study primarily demonstrates that αGalCer-stimulated NKT cells have a regulatory effect on osteoclastogenesis and a protective effect on inflammatory bone destruction. However, it also shows that these effects of αGalCer are diminished in RA patients, and that this is related to NKT cell dysfunction. These findings provide important information for those searching for novel therapeutic strategies to prevent bone destruction in RA. This article is protected by copyright. All rights reserved. © 2015, American College of Rheumatology.
    Arthritis and Rheumatology 06/2015; 67(10). DOI:10.1002/art.39244
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    ABSTRACT: Activation of NK cells is triggered by combined signals from multiple activating receptors that belong to different families. Several NK cell activating receptors have been identified, but their role in the regulation of effector functions is primarily understood in the context of their individual engagement. Therefore, little is known about the signaling pathways broadly implicated by the multiple NK cell activation cues. Here we provide evidence pointing to glycogen synthase kinase (GSK)-3β as a negative regulator of multiple NK cell activating signals. Using an activation model that combines NKG2D and 2B4 and tests different signaling molecules, we found that GSK-3 undergoes inhibitory phosphorylation at regulatory serine residues by the engagement of NKG2D and 2B4, either individually or in combination. The extent of such phosphorylation was closely correlated with the degree of NK cell activation. NK cell functions, such as cytokine production and cytotoxicity, were consistently enhanced by the knockdown of GSK-3β or its inhibition with different pharmacological inhibitors, whereas inhibition of the GSK-3α isoform had no effect. In addition, NK cell function was augmented by the overexpression of a catalytically inactive form of GSK-3β. Importantly, the regulation of NK cell function by GSK-3β was common to diverse activating receptors that signal through both ITAM and non-ITAM pathways. Thus, our results suggest that GSK-3β negatively regulates NK cell activation and that modulation of GSK-3β function could be used to enhance NK cell activation. Copyright © 2015. Published by Elsevier Inc.
    Cellular Signalling 05/2015; 27(9). DOI:10.1016/j.cellsig.2015.05.012 · 4.32 Impact Factor
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    ABSTRACT: Mucosal-associated invariant T (MAIT) cells contribute to protection against certain microorganism infections. The aims of this study were to examine the levels of MAIT cells in pulmonary tuberculosis (TB) and nontuberculous mycobacteria (NTM) lung disease patients, to evaluate the clinical relevance of MAIT cell levels, and to investigate the functions of MAIT cells. Patients with pulmonary TB (n = 35), NTM (n = 29), and healthy controls (n = 75) were enrolled in the study. MAIT cell levels and functions were measured by flow cytometry. Circluating MAIT cell levels were found to be reduced in TB and NTM patients. MAIT cell deficiency reflects a variety of clinical conditions. In particular, MAIT cell numbers were significantly correlated with sputum AFB positivity, extent of disease, hemoglobin levels, lymphocyte counts, CRP and ESR levels. MAIT cells in TB patients failed to produce interferon-γ irrespective of the mode of stimulation, whereas NTM patients displayed a defect in MR1-dependent signaling pathway. Notably, an elevated expression of programmed death-1 was also associated with MAIT cell deficiency in TB. This study shows that MAIT cells are numerically and functionally deficient in TB and NTM patients and these deficiencies could contribute to immune system dysreguation in mycobacterial infection. Copyright © 2015 Elsevier Ltd. All rights reserved.
    Tuberculosis (Edinburgh, Scotland) 03/2015; 161(3). DOI:10.1016/ · 2.71 Impact Factor
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    ABSTRACT: Mammalian sterile 20-like kinase 2 (Mst2) plays a central role in the Hippo pathway, controlling cell proliferation, differentiation, and apoptosis during development. However, the roles of Mst2 in osteoclast and osteoblast development are largely unknown. Here, we demonstrate that mice deficient in Mst2 exhibit osteoporotic phenotypes with increased numbers of osteoclasts and decreased numbers of osteoblasts as shown by micro-computed tomography (μCT) and histomorphometric analyses. Osteoclast precursors lacking Mst2 exhibit increased osteoclastogenesis and Nfatc1, Acp5, and Oscar expression in response to RANKL exposure. Conversely, Mst2 overexpression in osteoclast precursors leads to the inhibition of RANKL-induced osteoclast differentiation. Osteoblast precursors deficient in Mst2 exhibit attenuated osteoblast differentiation and function by downregulating the expression of Runx2, Alpl, Ibsp, and Bglap. Conversely, ectopic expression of Mst2 in osteoblast precursors increases osteoblastogenesis. Finally, we demonstrate that the NF-κB pathway is activated by Mst2 deficiency during osteoclast and osteoblast development. Our findings suggest that Mst2 is involved in bone homeostasis, functioning as a reciprocal regulator of osteoclast and osteoblast differentiation through the NF-κB pathway. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Journal of bone and mineral research: the official journal of the American Society for Bone and Mineral Research 03/2015; 30(9). DOI:10.1002/jbmr.2503 · 6.83 Impact Factor
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    ABSTRACT: Osteoclasts are unique cells responsible for the resorption of bone matrix. MicroRNAs (miRNAs) are involved in the regulation of a wide range of physiological processes. Here, we examined the role of miR-26a in RANKL-induced osteoclastogenesis. The expression of miR-26a was upregulated by RANKL at the late stage of osteoclastogenesis. Ectopic expression of an miR-26a mimic in osteoclast precursor cells attenuated osteoclast formation, actin-ring formation, and bone resorption by suppressing the expression of connective tissue growth factor/CCN family 2 (CTGF/CCN2), which can promote osteoclast formation via upregulation of dendritic cell-specific transmembrane protein (DC-STAMP). On the other hand, overexpression of miR-26a inhibitor enhanced RANKL-induced osteoclast formation and function as well as CTGF expression. In addition, the inhibitory effect of miR-26a on osteoclast formation and function was prevented by treatment with recombinant CTGF. Collectively, our results suggest that miR-26a modulates osteoclast formation and function through the regulation of CTGF.
    Molecules and Cells 12/2014; DOI:10.14348/molcells.2015.2241 · 2.09 Impact Factor
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    Jung Ha Kim · Nacksung Kim ·
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    ABSTRACT: Osteoclasts are unique cells that degrade the bone matrix. These large multinucleated cells differentiate from the monocyte/macrophage lineage upon stimulation by two essential cytokines, macrophage colony-stimulating factor (M-CSF) and receptor activator of nuclear factor-kappa B (NF-κB) ligand (RANKL). Activation of transcription factors such as microphthalmia transcription factor (MITF), c-Fos, NF-κB, and nuclear factor-activated T cells c1 (NFATc1) is required for sufficient osteoclast differentiation. In particular, NFATc1 plays the role of a master transcription regulator of osteoclast differentiation. To date, several mechanisms, including transcription, methylation, ubiquitination, acetylation, and non-coding RNAs, have been shown to regulate expression and activation of NFATc1. In this review, we have summarized the various mechanisms that control NFATc1 regulation during osteoclast differentiation.
    11/2014; 21(4):233-41. DOI:10.11005/jbm.2014.21.4.233
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    ABSTRACT: Mucosal-associated invariant T (MAIT) cells contribute to protection against certain microorganism infections and play an important role in mucosal immunity. However, the role of MAIT cells remains enigmatic in autoimmune diseases. In this study, we examined the level and function of MAIT cells in patients with rheumatic diseases. MAIT cell, cytokine, and programmed death-1 (PD-1) levels were measured by flow cytometry. Circulating MAIT cell levels were significantly reduced in systemic lupus erythematosus (SLE) and rheumatoid arthritis patients. In particular, this MAIT cell deficiency was more prominent in CD8(+) and double-negative T cell subsets, and significantly correlated with disease activity, such as SLE disease activity index and 28-joint disease activity score. Interestingly, MAIT cell frequency was significantly correlated with NKT cell frequency in SLE patients. IFN-γ production in MAIT cells was impaired in SLE patients, which was due to an intrinsic defect in the Ca(2+)/calcineurin/NFAT1 signaling pathway. In SLE patients, MAIT cells were poorly activated by α-galactosylceramide-stimulated NKT cells, thereby showing the dysfunction between MAIT cells and NKT cells. Notably, an elevated expression of PD-1 in MAIT cells and NKT cells was associated with SLE. In rheumatoid arthritis patients, MAIT cell levels were significantly higher in synovial fluid than in peripheral blood. Our study primarily demonstrates that MAIT cells are numerically and functionally deficient in SLE. In addition, we report a novel finding that this MAIT cell deficiency is associated with NKT cell deficiency and elevated PD-1 expression. These abnormalities possibly contribute to dysregulated mucosal immunity in SLE.
    The Journal of Immunology 09/2014; 193(8). DOI:10.4049/jimmunol.1302701 · 4.92 Impact Factor
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    ABSTRACT: Osteoblasts not only control bone formation but also support osteoclast differentiation. Here we show the involvement of Kruppel-like factor 4 (KLF4) in the differentiation of osteoclasts and osteoblasts. KLF4 was down-regulated by 1α,25-dihydroxyvitamin D3 (1,25(OH)2D3) in osteoblasts. Overexpression of KLF4 in osteoblasts attenuated 1,25(OH)2D3-induced osteoclast differentiation in co-culture of mouse bone marrow cells and osteoblasts through the down-regulation of receptor activator of nuclear factor κB ligand (RANKL) expression. Direct binding of KLF4 to the RANKL promoter repressed 1,25(OH)2D3-induced RANKL expression by preventing vitamin D receptor from binding to the RANKL promoter region. In contrast, ectopic overexpression of KLF4 in osteoblasts attenuated osteoblast differentiation and mineralization. KLF4 interacted directly with Runx2 and inhibited the expression of its target genes. Moreover, mice with conditional knockout of KLF4 in osteoblasts showed markedly increased bone mass caused by enhanced bone formation despite increased osteoclast activity. Thus, our data suggest that KLF4 controls bone homeostasis by negatively regulating both osteoclast and osteoblast differentiation.
    The Journal of Cell Biology 03/2014; 204(6). DOI:10.1083/jcb.201308102 · 9.83 Impact Factor

  • International journal of cardiology 01/2014; 172(3). DOI:10.1016/j.ijcard.2014.01.083 · 4.04 Impact Factor
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    ABSTRACT: Osteoblasts are specialized mesenchymal cells that are responsible for bone formation. In this study, we examine the role of GATA4 in osteoblast differentiation. GATA4 was abundantly expressed in preosteoblast cells and gradually down-regulated during osteoblast differentiation. Overexpression of GATA4 in osteoblastic cells inhibited alkaline phosphatase activity and nodule formation in osteogenic conditioned cell culture system. In addition, overexpression of GATA4 attenuated expression of osteogenic marker genes, including Runx2, alkaline phosphatase, bone sialoprotein, and osteocalcin, all of which are important for osteoblast differentiation and function. Overexpression of GATA4 attenuated Runx2 promoter activity, whereas silencing of GATA4 increased Runx2 induction. We found that GATA4 interacted with Dlx5 and subsequently decreased Dlx5 binding activity to Runx2 promoter region. Our data suggest that GATA4 acts as a negative regulator in osteoblast differentiation by downregulation of Runx2.
    BMB reports 12/2013; 47(8). DOI:10.5483/BMBRep.2014.47.8.225 · 2.60 Impact Factor
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    ABSTRACT: MicroRNAs (miRNAs) are endogenous non-coding 21–23 nucleotide RNAs that are involved in post-transcriptional regulation. They control various cellular processes, one of which is tumorigenesis. miRNAs have been implicated in the pathogenesis of hepatocellular carcinoma (HCC), the most common primary liver cancer. To find yet-to-be-identified miRNAs associated with HCC tumorigenesis, we resected HCC and adjacent non-tumor liver tissues from patients and excluded liver tissues harboring fibrosis from further analysis. We then carried out miRNA microarray analysis with miRNAs extracted from the tissues. Sixteen miRNAs displayed a significant change in expression levels between non-tumor and HCC liver tissues. To validate the microarray findings, we transfected HEK293 cells with miR-128 alone or miR-128 and plasmid encoding luciferase fused to the 3′ untranslated region (UTR) of E2F3, a predicted target of miR-128. As expected, miR-128 downregulated luciferase activities of E2F3 3′UTR fused to luciferase, confirming that E2F3 is a target gene of miR-128. Identification of miRNAs dysregulated in non-cirrhotic HCC will further the understanding of the pathogenesis of non-cirrhotic HCC.
    Genes & genomics 12/2013; 35(6). DOI:10.1007/s13258-013-0126-0 · 0.60 Impact Factor
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    ABSTRACT: Mucosal-associated invariant T (MAIT) cells have been reported to play an antimicrobial role in infectious diseases. However, little is known about age- and gender-related changes in circulating MAIT cell level and function in healthy population. The purposes of this study were to examine the level and cytokine production of circulating MAIT cells and their subsets in healthy adults and to investigate potential relationships between clinical parameters and MAIT cell levels or their subset levels. One hundred thirty-three healthy subjects were enrolled in this study. MAIT cells, their subset, and cytokine levels were measured by flow cytometry. Circulating MAIT cell levels were found to vary widely (0.19% to 21.7%) in the study subjects and to be significantly lower in elderly subjects (age, 61-92years) than in young subjects (age, 21-40years) (p<0.0005). No significant difference was found in the circulating MAIT cell levels between male and female subjects. A linear regression analysis revealed that circulating MAIT cell levels declined annually by 3.2% among men and 1.8% among women, respectively. Notably, the proportion of CD4+ MAIT cells increased with age, whereas that of CD8+ MAIT cells decreased with age. In addition, the production of interleukin (IL)-4 by MAIT cells was found to be significantly increased in elderly subjects and the ratio of interferon (IFN)-γ/IL-4 was lower as compared with young subjects, showing a Th1 to Th2 shift in cytokine profile in elderly subjects. Our data suggest that aging is associated with a reduction in circulating MAIT cells, accompanied with alterations in subset composition and cytokine profile.
    Experimental gerontology 11/2013; 49(1). DOI:10.1016/j.exger.2013.11.003 · 3.49 Impact Factor
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    ABSTRACT: RANKL induces the formation of osteoclasts, which are responsible for bone resorption. Herein, we investigated the role of SWAP-70-like adapter of T cells (SLAT) in RANKL-induced osteoclastogenesis. Expression levels of SLAT were reduced during RANKL-induced osteoclastogenesis. Overexpression of SLAT in BMMs inhibited TRAP-positive multinuclear osteoclast formation and attenuated the expression of NFATc1, which is an important modulator in osteoclastogenesis. Furthermore, silencing of SLAT by RNA interference enhanced osteoclast formation as well as NFATc1 expression. In addition, SLAT was involved in RANKL-induced JNK activation in osteoclasts. Taken together, our data suggest that SLAT acts as a negative modulator of RANKL-induced osteoclastogenesis.
    Molecules and Cells 08/2013; DOI:10.1007/s10059-013-0159-x · 2.09 Impact Factor
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    ABSTRACT: To examine the levels and functions of natural killer (NK) and natural killer T (NKT) cells, investigate relationships between NK and NKT cells, and determine the clinical relevance of NKT cell levels in patients with adult-onset Still's disease (AOSD). Patients with active untreated AOSD (n = 20) and age- and sex-matched healthy controls (n = 20) were studied. NK and NKT cell levels were measured by flow cytometry. Peripheral blood mononuclear cells were cultured in vitro with α-galactosylceramide (αGalCer). NK cytotoxicity against K562 cells and proliferation indices of NKT cells were estimated by flow cytometry. Percentages and absolute numbers of NKT cells were significantly lower in the peripheral blood of AOSD patients than in that of healthy controls. Proliferative responses of NKT cells to αGalCer were also lower in patients, and this was found to be due to proinflammatory cytokines and NKT cell apoptosis. In addition, NK cytotoxicity was found to be significantly lower in patients than in healthy controls, but NK cell levels were comparable in the 2 groups. Notably, this NKT cell deficiency was found to be correlated with NK cell dysfunction and to reflect active disease status. Furthermore, αGalCer-mediated NK cytotoxicity, showing the interaction between NK and NKT cells, was significantly lower in AOSD patients than in healthy controls. These findings demonstrate that NK and NKT cell functions are defective in AOSD patients and suggest that these abnormalities contribute to innate immune dysfunction in AOSD.
    Arthritis & Rheumatology 09/2012; 64(9):2868-77. DOI:10.1002/art.34514 · 7.76 Impact Factor
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    ABSTRACT: Natural killer T (NKT) cells have been reported to play crucial roles in a variety of diseases, including infectious diseases, autoimmunity, and cancers. Previous studies have reported wide age- and/or sex-related variations in circulating NKT cell levels in healthy subjects, but reported results are discrepant. In this study, the authors examined NKT cell levels in the peripheral blood of healthy Korean subjects and investigated potential relationships between clinical parameters and NKT cells and their subset levels. One hundred and thirty-eight age- and sex-matched healthy subjects were enrolled in this study. NKT cell and NKT subset levels were measured by flow cytometry. Circulating NKT cell levels were found to vary widely (0.01-5.15%) in the study subjects and to be lower in men than in women (P<0.05). Notably, gender-related differences in NKT cell levels were more prominent in elderly subjects (P<0.05). Furthermore, alterations in NKT subset compositions were found in elderly men, in whom the proportion of CD4+ NKT cells was elevated and that of double-negative NKT cells was reduced. Our data suggest that circulating NKT cells and NKT subset levels are affected by age and gender in the Korean population.
    Human immunology 08/2012; 73(10):1011-6. DOI:10.1016/j.humimm.2012.07.335 · 2.14 Impact Factor
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    ABSTRACT: Early growth response 2 (Egr2) is a zinc finger transcription factor that acts as an important modulator of various physiological processes. In this study, we show that Egr2 negatively regulates receptor activator of NF-κB ligand (RANKL)-induced osteoclast differentiation. The overexpression of Egr2 in bone marrow-derived macrophages (BMMs) suppresses the formation of multinuclear osteoclasts and the expression of osteoclastogenic markers, including nuclear factor of activated T cells c1 (NFATc1). On the other hand, Egr2 overexpression does not impact the phagocytic activity of osteoclast precursors or the expression of macrophage-specific markers in the presence of the osteoclastogenic stimuli, RANKL and M-CSF. We further demonstrate that Egr2 induces the expression of the inhibitors of differentiation/DNA binding (Ids) helix-loop-helix (HLH) transcription factors, which are important repressors in RANKL-mediated osteoclastogenesis. Egr2 transactivates the Id2 promoter and increases its recruitment to the Id2 promoter region. In addition, Egr2-dependent induction of Id2 promoter activity, and its binding to the Id2 promoter is abrogated by the overexpression of the Egr2 repressor, NGFI-A binding protein 2 (Nab2). Accordingly, coexpression with Nab2 restores Egr2-mediated suppression of osteoclast differentiation. Furthermore, knockdown of Egr2 using shRNA enhances osteoclastogenesis and decreases Id2 gene expression. Ectopic expression of Id2 reverses the phenotype mediated by Egr2 silencing. Taken together, our results identify Egr2 as an important modulator of RANKL-induced osteoclast differentiation and provide the link between RANKL, Egr2 and Id proteins in osteoclast-lineage cells.
    Bone 07/2012; 51(4):643-50. DOI:10.1016/j.bone.2012.07.015 · 3.97 Impact Factor
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    ABSTRACT: RANKL induces the formation of osteoclasts, which are responsible for bone resorption. Herein we investigate the role of the transmembrane adaptor proteins in RANKL-induced osteoclastogenesis. LAT positively regulates osteoclast differentiation and is up-regulated by RANKL via c-Fos and NFATc1, whereas LAB and LIME act as negative modulators of osteoclastogenesis. In addition, silencing of LAT by RNA interference or overexpression of a LAT dominant negative in bone marrow-derived macrophage cells attenuates RANKL-induced osteoclast formation. Furthermore, LAT is involved in RANKL-induced PLC(γ) activation and NFATc1 induction. Thus, our data suggest that LAT acts as a positive regulator of RANKL-induced osteoclastogenesis.
    Molecules and Cells 02/2012; 33(4):401-6. DOI:10.1007/s10059-012-0009-2 · 2.09 Impact Factor
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    Nacksung Kim · Hong Yong Park · Hyun Dong Kim ·
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    ABSTRACT: Osteoclasts are multinucleated giant cells which can resorb bone and differentiated from hematopoietic cells. We have previously reported murine osteoclast-associated receptor (OSCAR) may be an important bone-specific regulator of osteoclast differentiation. We have cloned soluble form of human OSCAR (hOSCAR) and examined the role of hOSCAR on osteoclast differentiation.
    01/2012; 19(1):11. DOI:10.11005/kjbm.2012.19.1.11
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    ABSTRACT: SHIP is an SH2-containing inositol-5-phosphatase expressed in hematopoietic cells. It hydrolyzes the PI3K product PI(3,4,5)P(3) and blunts the PI3K-initiated signaling pathway. Although the PI3K/Akt pathway has been shown to be important for osteoclastogenesis, the molecular events involved in osteoclast differentiation have not been revealed. We demonstrate that Akt induces osteoclast differentiation through regulating the GSK3β/NFATc1 signaling cascade. Inhibition of the PI3K by LY294002 reduces formation of osteoclasts and attenuates the expression of NFATc1, but not that of c-Fos. Conversely, overexpression of Akt in bone marrow-derived macrophages (BMMs) strongly induced NFATc1 expression without affecting c-Fos expression, suggesting that PI3K/Akt-mediated NFATc1 induction is independent of c-Fos during RANKL-induced osteoclastogenesis. In addition, we found that overexpression of Akt enhances formation of an inactive form of GSK3β (phospho-GSK3β) and nuclear localization of NFATc1, and that overexpression of a constitutively active form of GSK3β attenuates osteoclast formation through downregulation of NFATc1. Furthermore, BMMs from SHIP knockout mice show the increased expression levels of phospho-Akt and phospho-GSK3β, as well as the enhanced osteoclastogenesis, compared with wild type. However, overexpression of a constitutively active form of GSK3β attenuates RANKL-induced osteoclast differentiation from SHIP-deficient BMMs. Our data suggest that the PI3K/Akt/GSK3β/NFATc1 signaling axis plays an important role in RANKL-induced osteoclastogenesis.
    The Journal of Immunology 11/2011; 188(1):163-9. DOI:10.4049/jimmunol.1101254 · 4.92 Impact Factor

Publication Stats

4k Citations
407.86 Total Impact Points


  • 2005-2015
    • Chonnam National University
      • Department of Pharmacology
      Gwangju, Gwangju, South Korea
    • Ewha Womans University
      • Center for Cell Signaling Research (CCSR)
      Sŏul, Seoul, South Korea
  • 2011-2013
    • Chonnam National University Hospital
      Sŏul, Seoul, South Korea
  • 2010
    • Chungnam National University
      • Department of Microbiology
      Sŏngnam, Gyeonggi Province, South Korea
  • 2003
    • University of Pennsylvania
      • Department of Pathology and Laboratory Medicine
      Philadelphia, PA, United States
  • 2000-2002
    • The Rockefeller University
      • Laboratory of Molecular Biology
      New York, New York, United States