Faculty Profiles - TAKIGAWA Masaharu

Papers - TAKIGAWA Masaharu

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Downregulation of a rheumatoid arthritis-related antigen (RA-A47) by ra-a47 antisense oligonucleotides induces inflammatory factors in chondrocytes

T Hattori, H Kawaki, S Kubota, Y Yutani, B De Crombrugghe, K Von Der Mark, M Takigawa

JOURNAL OF CELLULAR PHYSIOLOGY 197 ( 1 ) 94 - 102 2003.10

Language：English Publishing type：Research paper (scientific journal) Publisher：WILEY-BLACKWELL

Previously we have shown that the expression of RA-A47 (rheumatoid arthritis-related antigen) which is identical to HSP47, a collagen-binding chaperon, is downregulated in chondrocytes by tumor necrosis factor alpha (TNFalpha). RA-A47 was also found on the surface of chondrocytes where it is recognized as an antigen in the serum of rheumatoid arthritis (RA) patients. Its translocation to the cell surface from endoplasmic reticulum membrane where it is normally located was also enhanced by TNFalpha. To understand the significance of RA-A47 downregulation in chondrocytes independent from other effects of TNFalpha, we used an antisense oligonucleotide approach and investigated the effect of this treatment on the expression of molecules related to matrix degradation and production of growth factors for chondrocytic, endothelial, and synovial cells. Here we show that treatment of rabbit chondrocyes and human chondrosarcoma cells HCS-2/8 by ra-a47 antisense S-oligonucleotides significantly reduced the expression of ra-a47 both at mRNA and protein level. Interestingly, this TNFalpha-independent RA-A47 clownregulation was associated with a strong induction of matrix metalloproteinase (MMP)-9 mRNA and inducible NO synthase (iNOS) mRNA. The induction of active-type MMP-9 was further detected by gelatin zymography. Under the same conditions, the release of basic fibroblast growth factor (bFGF) and connective tissue growth factor (CTGF) from HCS-2/8 cells into the conditioned medium (CM) was strongly enhanced. These effects were not a result of TNFalpha upregulation, since the ra-a47 antisense oligonucleotide treatment did not enhance TNFalpha synthesis. These observations indicate that clownregulation of RA-A47 induces TNFalpha-independent cartilage-degrading pathways involving iNOS and MMP-9. Furthermore, the stimulation of bFGF and CTGF release from chondrocytes may stimulate the proliferation of adjacent endothelial and/or synovial cells. (C) 2003 Wiley-Liss, Inc.

DOI： 10.1002/jcp.10341

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CTGFは軟骨においてI型コラーゲンと共発現する

福永智広, 山城隆, 大矢伸治, 竹下信郎, 滝川正春, 山本照子

日本矯正歯科学会大会プログラム・抄録集 62回 201 - 201 2003.10

A repetitive, steady mouth opening induced an osteoarthritis-like lesion in the rabbit temporomandibular joint

T Fujisawa, T Kuboki, T Kasai, W Sonoyama, S Kojima, J Uehara, C Komori, H Yatani, Hattori, I, M Takigawa

JOURNAL OF DENTAL RESEARCH 82 ( 9 ) 731 - 735 2003.9

Language：English Publishing type：Research paper (scientific journal) Publisher：INT AMER ASSOC DENTAL RESEARCHI A D R/A A D R

Although excessive mechanical stress is assumed to be one of the factors contributing to pathogenesis of temporomandibular joint (TMJ) osteoarthritis (OA), no pure mechanical-stress-induced OA model has been developed without surgical manipulation or puncture of the joint cavity. The purpose of this study was to establish a genuine mechanical-stress-induced OA model of the rabbit TMJ. In the experimental rabbits, repetitive, forced jaw-opening, 3 hrs/day for 5 days, was applied with the use of a general anesthesia protocol. By histological assessment of the TMJ articular tissues, partial eburnation of the articular cartilage, reactive marginal proliferation of the articular cartilage chondrocytes, and nested proliferation of chondrocytes in the subchondral bone area were observed at 7 days after the repetitive, forced-jaw-opening period. These results suggest that the repetitive, forced-jaw-opening protocol without surgical intervention can induce evident OA-like lesions in the rabbit TMJ, and this OA model may greatly contribute to the elucidation of the cartilage degradation mechanism in TMJ OA.

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CTGF/Hcs24/CCN2, hypertrophic chondrocyte-specific gene product, interacts with perlecan in regulating the proliferation and differentiation of chondrocytes.

T Nishida, S Kubota, T Fukunaga, S Kondo, G Yosimichi, T Nakanishi, T Takano-Yamamoto, M Takigawa

JOURNAL OF BONE AND MINERAL RESEARCH 18 S108 - S108 2003.9

CTGF/Hcs24, hypertrophic chondrocyte-specific gene product, interacts with perlecan in regulating the proliferation and differentiation of chondrocytes Reviewed

T Nishida, S Kubota, T Fukunaga, S Kondo, G Yosimichi, T Nakanishi, T Takano-Yamamoto, M Takigawa

JOURNAL OF CELLULAR PHYSIOLOGY 196 ( 2 ) 265 - 275 2003.8

Language：English Publishing type：Research paper (scientific journal) Publisher：WILEY-LISS

Connective tissue growth factor/hypertrophic chondrocyte-specific gene product 24 (CTGF/Hcs24) plays important roles in the control of the proliferation and differentiation of chondrocytes in vitro. To clarify the mechanisms of regulation by CTGF/Hcs24 with respect to cartilage metabolism, we investigated the interaction between CTGF/Hcs24 and heparan sulfate proteoglycan perlecan. An immunofluorescence study showed that CTGF/Hcs24 was colocalized with heparan sulfate and perlecan in human chondrosarcoma-derived chondrocytic cell line HCS-2/8 in vitro. Northern blot analysis showed that perlecan, syndecan-1, -2, and -4 transcripts were detected in HCS-2/8 cells. Particularly, expression of the perlecan gene increased markedly in HCS-2/8 cells by recombinant CTGF/Hcs24 (rCTGF/Hcs24) treatment. We also found that CTGF/Hcs24 interacted with perlecan from HCS-2/8 cells in vitro. Furthermore, CTGF/Hcs24-stimulated gene expression of the aggrecan gene, as well as DNA/proteoglycan synthesis, was diminished when HCS-2/8 cells were pretreated with heparinase, indicating that the effects of CTGF/Hcs24 on chondrocytes occurred through the interaction between CTGF/Hcs24 and heparan sulfate on the cells. An in vivo study using mouse growth plate revealed that CTGF/Hcs24 produced by hypertrophic chondrocytes was localized from the proliferative to the hypertrophic zone, whereas perlecan was predominantly localized in the prehyphertrophic zone. Consistent with such findings in vivo, the binding of I-125-rCTGF/Hcs24 to maturing chondrocytes was at higher levels than that to chondrocytes in hypertrophic stages. These findings suggest that CTGF/Hcs24 produced in the hypertrophic region may act on chondrocytes in the proliferative and maturative zone via some heparan sulfate proteoglycan, such as perlecan. (C) 2003 Wiley-Liss, Inc.

DOI： 10.1002/jpc.10277

ヒト軟骨肉腫培養細胞株における結合組織成長因子(CTGF)の低酸素による誘導はp38 MAPK経路を介している

近藤誠二, 久保田聡, 森谷徳文, 滝川正春

日本癌学会総会記事 62回 86 - 86 2003.8

Cbfa1/Runx2 gene expression in articular chondrocytes of the mice temporomandibular and knee joints in vivo

T Kuboki, M Kanyama, T Nakanishi, K Akiyama, K Nawachi, H Yatani, K Yamashita, T Takano-Yamamoto, M Takigawa

ARCHIVES OF ORAL BIOLOGY 48 ( 7 ) 519 - 525 2003.7

Language：English Publishing type：Research paper (scientific journal) Publisher：PERGAMON-ELSEVIER SCIENCE LTD

Healthy articular cartilage is thought to be maintained by the modulation of Cbfa1 expression, although little is currently known about Cbfa1 expression in such tissues. Therefore, we examined in vivo Cbfa1 transcript levels in the temporomandibular (TM) and knee joints of 3- and 10-week-old mate ICR mice (weighing 50-70 g). A digoxigenin-11-UTP-labeled single-stranded RNA probe (0.6 kbp PstI-HindIII fragment of the 3' of untranslated region in exon 8 of mouse Cbfa1 cDNA) was prepared and in situ hybridization was performed on paraffin-embedded TM and knee joint sections. The antisense probe detected Cbfa1 transcripts in prehypertrophic chondrocytes, but not in the articular surface layer chondrocytes, of 3- and 10-week-old mice TMJs. Despite the intense Cbfa1 expression in prehypertrophic chondrocytes, articular surface layer chondrocytes of the knee joints expressed tow and undetectable level of Cbfa1 in the 3- and 10-week-old mice, respectively. These results indicate that Cbfa1 are highly expressed in the prehypertrophic chondrocytes presumably for articular tissue remodeling during the entire lifespan of the mouse, whereas Cbfa1 expression is suppressed in the articular surface chondrocytes in the adult mouse TM and knee joints to obtain the permanent cartilage phenotype. (C) 2003 Elsevier Science Ltd. All rights reserved.

DOI： 10.1016/S0003-9969(03)00088-8

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Transcriptional induction of connective tissue growth factor hypertrophic chondrocyte-specific 24 gene by dexamethasone in human chondrocytic cells

S Kubota, NH Moritami, H Kawaki, H Mimura, M Minato, M Takigawa

BONE 32 ( 5 ) S98 - S98 2003.5

Proposal for a unified CCN nomenclature

DR Brigstock, R Goldschmeding, K Katsube, SCT Lam, LF Lau, K Lyons, C Naus, B Perbal, B Riser, M Takigawa, H Yeger

JOURNAL OF CLINICAL PATHOLOGY-MOLECULAR PATHOLOGY 56 ( 2 ) 127 - 128 2003.4

Language：English Publishing type：Research paper (scientific journal) Publisher：BRITISH MED JOURNAL PUBL GROUP

A proposal is put forth to unify the nomenclature of the CCN family of secreted, cysteine rich regulatory proteins. In the order of their description in the literature, CCN1 (CYR61), CCN2 (CTGF), CCN3 (NOV), CCN4 (WISP-1), CCN5 (WISP-2), and CCN6 (WISP-3) constitute a family of matricellular proteins that regulate cell adhesion, migration, proliferation, survival, and differentiation, at least in part through integrin mediated mechanisms. This proposal is endorsed by the International CCN Society and will serve to eliminate confusion from the multiple names that have been given to these molecules.

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顎関節ならびに膝関節の関節軟骨におけるCbfα1/Runx2遺伝子の発現

窪木拓男, 完山学, 中西徹, 秋山謙太郎, 縄稚久美子, 矢谷博文, 山下和夫, 山本照子, 滝川正春

日本顎関節学会雑誌 15 ( 1 ) 112 - 112 2003.4

Suppressive effect of overexpressed connective tissue growth factor on tumor cell growth in a human oral squamous cell carcinoma-derived cell line

NH Moritani, S Kubota, T Nishida, H Kawaki, S Kondo, T Sugahara, M Takigawa

CANCER LETTERS 192 ( 2 ) 205 - 214 2003.3

Language：English Publishing type：Research paper (scientific journal) Publisher：ELSEVIER SCI IRELAND LTD

Connective tissue growth factor (CTGF) is known to be a multifunctional growth factor that is overexpressed. in several types of malignancies. In this study, effects of CTGF gene overexpression on the phenotypes of oral squamous cell carcinoma cells were investigated by using a cell line with undetectable endogenous CTGF expression. Surprisingly, our results indicated that CTGF-overexpressed clones were characterized by attenuated cell growth and less potent tumorigenicity, with coincidental downregulation of prothymosin a gene. Although CTGF is known to promote cell proliferation in mesenchymal cells, our present results suggest that CTGF acts as a negative regulator of the cell growth in oral squamous cell carcinoma possibly through its interaction with growth modifiers inside the cell. (C) 2003 Elsevier Science Ireland Ltd. All rights reserved.

DOI： 10.1016/S0304-3835(02)00718-8

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Role of CTGF/HCS24/ecogenin in skeletal growth control

M Takigawa, T Nakanishi, S Kubota, T Nishida

JOURNAL OF CELLULAR PHYSIOLOGY 194 ( 3 ) 256 - 266 2003.3

Language：English Publisher：WILEY-LISS

Connective tissue growth factor/hypertrophic chondrocyte-specific gene product 24 (CTGF/Hcs24) is a multifunctional growth factor for chondrocytes, osteoblasts, and vascular endothelial cells. CTGF/Hcs24 promotes the proliferation and maturation of growth cartilage cells and articular cartilage cells in culture and hypertrophy of growth cartilage cells in culture. The factor also stimulates the proliferation and differentiation of cultured osteoblastic cells. Moreover, CTGF/Hcs24 promotes the adhesion, proliferation, and migration of vascular endothelial cells, as well as induces tube formation by the cells and strong angiogenesis in vivo. Because angiogenesis is critical for the replacement of cartilage with bone at the final stage of endochondral ossification and because gene expression of CTGF/Hcs24 predominates in hypertrophic chondrocytes in the physiological state, a major physiological role for this factor should be the promotion of the entire process of endochondral ossification, with the factor acting on the above three types of cells as a paracrine factor. Thus, CTGF/Hcs24 should be called "ecogenin: endochondral ossification genetic factor." In addition to hypertrophic chondrocytes, osteoblasts activated by various stimuli including wounding also express a significantly high level of CTGF/Hcs24. These findings in conjunction with in vitro findings about osteoblasts mentioned above suggest the involvement of CTGF/Hcs24 in intramembranous ossification and bone modeling/remodeling. Because angiogenesis is also critical for intramembranous ossification and bone remodeling, CTGF/Hcs24 expressed in endothelial cells activated by various stimuli including wounding may also play important roles in direct bone formation. In conclusion, although the most important physiological role of CTGF/Hcs24 is ecogenin action, the factors also play important roles in skeletal growth and modeling/remodeling via its direct action on osteoblasts under both physiological and pathological conditions. (C) 2003 Wiley-Liss, Inc.

DOI： 10.1002/jcp.10206

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CTGF/Hcs24 as a multifunctional growth factor for fibroblasts, chondrocytes and vascular endothelial cells

M Takigawa

DRUG NEWS & PERSPECTIVES 16 ( 1 ) 11 - 21 2003.1

Language：English Publisher：PROUS SCIENCE, SA-THOMSON REUTERS

Connective tissue growth factor/hypertrophic chondrocyte-specific gene product 24 (CTGF/Hcs24), a member of the CCN family, is a multifunctional growth factor for fibroblasts, chondrocytes and vascular endothelial cells. Depending on the type of cell with which it interacts, it promotes chemotaxis, migration, adhesion, proliferation, differentiation and/or extracellular matrix formation. Because gene expression of CTGF/Hcs24 is maximal in hypertrophic chondrocytes in the physiological state, a major physiological role for this factor should be the promotion of endochondral ossification. On the other hand, its expression is up-regulated during wound healing, indicating the involvement of this factor in this process as well. When overexpressed, CTGF/Hcs24 may cause pathological states such as fibrotic disorders and angiogenic diseases. This review focuses on the physiological and pathological significances of his novel type of growth factor. (C) 2003 Prous Science. All rights reserved.

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Conserved repressive regulation of connective tissue growth factor/hypertrophic chondrocyte-specific gene 24 (ctgf/hcs24) enabled by different elements and factors among vertebrate species

Y Mukudai, S Kubota, M Takigawa

BIOLOGICAL CHEMISTRY 384 ( 1 ) 1 - 9 2003.1

Language：English Publishing type：Research paper (scientific journal) Publisher：WALTER DE GRUYTER & CO

CTGF/Hcs24 is a multifunctional growth factor that potentiates the growth and differentiation of various cells. Our previous study revealed that the 3'-UTR of mammalian CTGF/Hcs24 mRNA contains a small segment that represses the gene expression in cis fashion. In this study, we isolated and characterized a chicken CTGF/Hcs24 cDNA clone. Chicken ctgf/hcs24 mRNA showed highly conserved homology in the ORF to that of mammalian species, whereas the homology in the 3'-UTR was relatively low. Northern blotting analysis revealed that chicken ctgf/hcs24 mRNA was expressed most strongly in cartilage, and also in brain, lung, heart, but faintly in liver. Thereafter we analyzed the functional potential of the 3'-UTR of ctgf/hcs24 cDNA to regulate its gene expression by reporter gene assay, and found that it repressed gene expression in cis fashion, specifically in avian cells, but not in mammalian cells. Conversely, the mammalian 3'-UTR showed less repressive activity in avian cells than in mammalian cells. Deletion analysis showed that a segment near the polyadenyl tail of the 3'-UTR of chicken ctgf/hcs24 played an important functional role, unlike in the mammalian species. Thus, we uncovered a novel mode of functional conservation of the ctgf/hcs24 3'-UTR among vertebrate species mediated by different factors.

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成長因子と軟骨細胞 Invited

久保田聡, 滝川正春

腎と骨代謝 16, 103-110 2003

Interaction of AP-1 and the ctgf gene: a possible driver of chondrocyte hypertrophy in growth cartilage

NH Moritani, S Kubota, T Eguchi, T Fukunaga, T Yamashiro, T Takano-Yamamoto, H Tahara, K Ohyama, T Sugahara, M Takigawa

JOURNAL OF BONE AND MINERAL METABOLISM 21 ( 4 ) 205 - 210 2003

Language：English Publishing type：Research paper (scientific journal) Publisher：SPRINGER-VERLAG TOKYO

The expression of the connective tissue growth factor (ctgf) gene increases along with the differentiation of growth cartilage cells, and the highest expression is observed in the hypertrophic stage. Similarly, recent reports demonstrated c-fos expression in chondrocytes in the early hypertrophic zone of growth cartilage, and suggested that the c-fos gene may play a crucial role in the regulation of hypertrophic differentiation. A chondrocytic human cell line, HCS-2/8, is known to retain a variety of chondrocytic phenotypes. When such cells were kept overconfluent, they expressed increasing levels of c-fos transcripts along a time course phenotypically similar to that of hypertrophic differentiation. Moreover, by using a competitive electromobility-shift assay, we found that AP-1, a Fos/Jun heterodimer, in HCS-2/8 was capable of binding not only to a typical AP-1-binding DNA fragment but also to the enhancer fragment of the ctgf gene. Based on the findings above, we hypothesize that, prior to hypertrophic differentiation, AP-1-related oncogenes are activated and that their gene products subsequently activate ctgf gene expression, which might eventually induce hypertrophy.

DOI： 10.1007/s00774-003-0410-1

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Gene expression profiles in chondrosarcoma cells subjected to cyclic stretching and hydrostatic pressure. A cDNA array study

HM Karjalainen, RK Sironen, MA Elo, K Kaarniranta, M Takigawa, HJ Helminen, MJ Lammi

BIORHEOLOGY 40 ( 1-3 ) 93 - 100 2003

Language：English Publishing type：Research paper (scientific journal) Publisher：IOS PRESS

Mechanical forces have a profound effect on cartilage tissue and chondrocyte metabolism. Strenuous loading inhibits the cellular metabolism, while optimal level of loading at correct frequency raises an anabolic response in chondrocytes. In this study, we used Atlas Human Cancer cDNA array to investigate mRNA expression profiles in human chondrosarcoma cells stretched 8% for 6 hours at a frequency of 0.5 Hz. In addition, cultures were exposed to continuous and cyclic (0.5 Hz) 5 MPa hydrostatic pressure. Cyclic stretch had a more profound effect on the gene expression profiles than 5 MPa hydrostatic pressure. Several genes involved with the regulation of cell cycle were increased in stretched cells, as well as mRNAs for PDGF-B, glucose-1-phosphate uridylyltransferase, Tiam1, cdc37 homolog, Gem, integrin alpha(6), and matrix metalloproteinase-3. Among down-regulated genes were plakoglobin, TGF-alpha, retinoic acid receptor-alpha and Wnt8b. A smaller number of changes was detected after pressure treatments. Plakoglobin was increased under cyclic and continuous 5 MPa hydrostatic pressure, while mitogen-activated protein kinase-9, proliferating cell nuclear antigen, Rad6, CD9 antigen, integrins alpha(E) and beta(8), and vimentin were decreased. Cyclic and continuous pressurization induces a number of specific changes. In conclusion, a different set of genes were affected by three different types of mechanical stimuli applied on chondrosarcoma cells.

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Hepatocyte growth factor counteracts transforming growth factor-beta1, through attenuation of connective tissue growth factor induction, and prevents renal fibrogenesis in 5/6 nephrectomized mice.

Inoue T, Okada H, Kobayashi T, Watanabe Y, Kanno Y, Kopp J B, Nishida T, Takigawa M, Ueno M, Nakamura T, Suzuki H

FASEB J 17, 268 - 270, 2003

CTGF/Hcs24 interacts with the cytoskeletal protein actin in chondrocytes

G Yosimichi, S Kubota, T Hattori, T Nishida, K Nawachi, T Nakanishi, M Kamada, T Takano-Yamamoto, M Takigawa

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 299 ( 5 ) 755 - 761 2002.12

Language：English Publishing type：Research paper (scientific journal) Publisher：ACADEMIC PRESS INC ELSEVIER SCIENCE

Connective tissue growth factor/hypertrophic chondrocyte-specific gene product 24 (CTGF/Hcs24) displays multiple functions in several types of mesenchymal cells, including the promotion of proliferation and differentiation of chondrocytes. Recently, the internalization and intracellular function of CTGF/Hcs24 were indicated as well. In this study, a binding protein for this factor was purified from the cytosolic fraction of human chondrosarcoma-derived chondrocytic cell line (HCS-2/8) by CTGF/Hcs24-affinity chromatography. The apparent molecular weight of the protein was 42 kDa and determination of the internal amino acid sequence revealed this protein to be beta- or gamma-actin. An in vitro competitive binding assay of I-125-labeled recombinant CTGF/Hcs24 with cold-rCTGF/Hcs24 showed that the binding between actin and I-125-CTGF/Hcs24 was specific. Immunoprecipitation analysis also showed that CTGF/Hcs24 bound to actin in HCS-2/8 cells. However, rCTGF/Hcs24 had no effects on the expression level of gamma-actin mRNA or total actin protein. These findings suggest that a significant portion of intracellular CTGF/Hcs24 may regulate certain cell biological events in chondrocytes through the interaction with this particular cytoskeletal protein. (C) 2002 Elsevier Science (USA). All rights reserved.

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CD44 stimulation by fragmented hyaluronic acid induces upregulation of urokinase-type plasminogen activator and its receptor and subsequently facilitates invasion of human chondrosarcoma cells

H Kobayashi, M Suzuki, N Kanayama, T Nishida, M Takigawa, T Terao

INTERNATIONAL JOURNAL OF CANCER 102 ( 4 ) 379 - 389 2002.12

Language：English Publishing type：Research paper (scientific journal) Publisher：WILEY-BLACKWELL

It has been established that fragmented hyaluronic acid (HA), but not native high molecular weight HA, can induce angiogenesis, cell proliferation and migration. We have studied the outside-in signal transduction pathways responsible for fragmented HA-mediated cancer cell invasion. In our study, we have studied the effects of CD44 stimulation by ligation with HA upon the expression of matrix metalloproteinases (MMPs)-2 and -9 as well as urokinase-type plasminogen activator (uPA), its receptor (uPAR) and its inhibitor (PAI-1) and the subsequent induction of invasion of human chondrosarcoma cell line HCS-2/8. Our study indicates that (i) CD44 stimulation by fragmented HA upregulates expression of uPA and uPAR mRNA and protein but does not affect MMPs secretion or PAW mRNA expression; (ii) the effects of HA fragments are critically HA size dependent: high molecular weight HA is inactive, but lower molecular weight fragmented HA (Mr 33 kDa) is active; (iii) cells can bind avidly Mr 3.5 kDa fragmented HA through a CD44 molecule, whereas cells do not effectively bind higher Mr HA; (iv) a fragmented HA induces phosphorylation of MAP kinase proteins (MEK1/2, ERK1/2 and c-Jun) within 30 min; (v) CD44 is critical for the response (activation of MAP kinase and upregulation of uPA and uPAR expression); and (vi) cell invasion induced by CD44 stimulation with a fragmented HA is inhibited by anti-CD44 mAb, MAP kinase inhibitors, neutralizing anti-uPAR pAb, anti-catalytic anti-uPA mAb or amiloride. Therefore, our study represents the first report that CD44 stimulation induced by a fragmented HA results in activation of MAP kinase and, subsequently, enhances uPA and uPAR expression and facilitates invasion of human chondrosarcoma cells. (C) 2002 Wiley-Liss, Inc.

DOI： 10.1002/ijc.10710

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