Faculty Profiles - TAKIGAWA Masaharu

Papers - TAKIGAWA Masaharu

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軟骨細胞におけるチロシンキナーゼ型レセプターErbB4遺伝子の発現

縄稚久美子, 久保田聡, 井上美穂, 西田崇, 吉道玄, 中西徹, 完山学, 窪木拓男, 矢谷博文, 山合友一郎, 滝川正春

日本骨形態計測学会雑誌 12 ( 3 ) 63 - 63 2002.12

軟骨細胞におけるチロシンキナーゼ型レセプターErbB4遺伝子の発現

縄稚久美子, 久保田聡, 井上美穂, 西田崇, 吉道玄, 中西徹, 完山学, 窪木拓男, 矢谷博文, 山合友一郎, 滝川正春

生化学 74 ( 11 ) 1413 - 1413 2002.11

Expression of connective tissue growth factor/hypertrophic chondrocyte-specific gene product 24 (CTGF/Hcs24) during fracture healing

E Nakata, T Nakanishi, A Kawai, K Asaumi, T Yamaai, M Asano, T Nishida, S Mitani, H Inoue, M Takigawa

BONE 31 ( 4 ) 441 - 447 2002.10

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

Localization and expression of connective tissue growth factor/hypertrophic chondrocyte-specific gene product 24 (CTGF/Hcs24) during fracture healing in mouse ribs were investigated. In situ hybridization demonstrated that CTGF/Hcs24 mRNA was remarkably expressed, especially in hypertrophic chondrocytes and proliferating chondrocytes, in the regions of regenerating cartilage on days 8 and 14 after fracture. CTGF/Hcs24 mRNA was also expressed in proliferating periosteal cells in the vicinity of the fracture sites on days 2 and 8, and in cells in fibrous tissue around the callus on day 8. Northern blot analysis showed that expression of CTGF/Hcs24 mRNA was 3.9 times higher on day 2 of fracture healing than that on day 0. On day 8, it reached a peak of 8.6 times higher than that on day 0. It then declined to a lower level. Immunostaining showed that CTGF/Hcs24 was localized in hypertrophic chondrocytes and proliferating chondrocytes in the regions of regenerating cartilage, and in active osteoblasts in the regions of intramembranous ossification. Although CTGF/Hcs24 was abundant in the proliferating and differentiating cells (on days 8 and 14), immunostaining decreased as the cells differentiated to form bone (on day 20). CTGF/Hcs24 was also detected in cells in fibrous tissue, vascular endothelial cells in the callus, and periosteal cells around the fracture sites. These results suggest that CTGF/Hcs24 plays some role in fracture healing.

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ラット下顎枝骨折治癒過程の膜性骨化と内軟骨性骨化における結合組織成長因子(CTGF)の経時的発現

福永智広, 山城隆, 小橋紀之, 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 61回 165 - 165 2002.10

Tyrosine kinase-type receptor ErbB4 in chondrocytes: interaction with connective tissue growth factor and distribution in cartilage

K Nawachi, M Inoue, S Kubota, T Nishida, G Yosimichi, T Nakanishi, M Kanyama, T Kuboki, H Yatani, T Yamaai, M Takigawa

FEBS LETTERS 528 ( 1-3 ) 109 - 113 2002.9

Language：English Publishing type：Research paper (scientific journal) Publisher：ELSEVIER SCIENCE BV

In order to identify receptor molecules that participate in the growth and differentiation of cliondrocytes, we cloned a number of cDNA fragments from HCS-2/8 chondrocytic cells, by using tyrosine kinase-specific primers for amplification. The mRNA expression of one such receptor, ErbB4, was increased by connective tissue growth factorthypertrophic chondrocyte-specific gene product (CTGF/Hes24), which promotes all stages of the endochondral ossification in vitro. ErbB4 expression was observed through all stages of chondrocytic differentiation in vitro, corresponding to the wide distribution of CTGF/Hcs24 target cells. Furthermore, positive signals for erbB4 mRNA were detectable throughout most populations of chondrocytes, in growth and articular cartilage in vivo. These results demonstrate for the first time that ErbB4 is expressed in chondrocytes and may play some roles in chondrocytic growth and differentiation along with CTGF/Hcs24. (C) 2002 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.

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TGF-beta 1 and HGF coordinately facilitate collagen turnover in subepithelial mesenchyme

T Inoue, H Okada, T Kobayashi, Y Watanabe, T Kikuta, Y Kanno, M Takigawa, H Suzuki

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 297 ( 2 ) 255 - 260 2002.9

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

We have employed co-culture of proximal tubular epithelial cells (PTEC) and renal tubulo-interstitial fibroblasts (TFB) to study the role of transforming growth factor-beta1 (TGF-beta1) and hepatocyte growth factor (HGF) in epithelial-mesenchymal interactions. In co-culture, TGF-beta1 stimulated TFB to produce type I collagen (COLI). This effect was both direct and indirect, via connective tissue growth factor (CTGF) produced by the co-cultured PTEC. Co-administration of TGF-beta1 and HGF significantly increased overall COLI production by TFB by 24 h. However, in detail, this co-administration enhanced CTGF induction in PTEC during the first 8 h, and then decreased its expression, resulting in a rapid decrease in expression of the alpha1 (1) procollagen gene in TFB by 24 h. Additionally, tissue inhibitor of metalloproteinase-1 was induced in PTEC by TGF-beta1 with or without co-administration of HGF, which contributed to the COLI accumulation. In contrast, HGF alone or co-administered with TGF-beta1 significantly increased collagenolytic activity derived from PTEC. Therefore, TGF-beta1 and HGF seem to coordinately modulate epithelial-mesenchymal interactions to facilitate COLI turnover in subepithelial mesenchyme. (C) 2002 Elsevier Science (USA). All rights reserved.

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Possible roles of CTGF/Hcs24 in the initiation and development of ossification of the posterior longitudinal ligament

Y Yamamoto, KI Furukawa, K Ueyama, T Nakanishi, M Takigawa, S Harata

SPINE 27 ( 17 ) 1852 - 1857 2002.9

Language：English Publishing type：Research paper (scientific journal) Publisher：LIPPINCOTT WILLIAMS & WILKINS

Study Design. A biochemical and histochemical study investigating the role of CTGF/Hcs24 in the ossification of the posterior longitudinal ligament (OPLL) was conducted.
Objective. To clarify the involvement of CTGF/Hcs24 in ectopic bone formation in OPLL through endochondral ossification using human tissue.
Summary of Background Data. Previous studies have shown that various cytokines are involved in the occurrence or development of ectopic bone formation in OPLL. Recently, the authors cloned an mRNA predominantly expressed in chondrocytes by differential display PCR and found,that it's gene, hcs24, is identical to that of connective tissue growth factor. It has been shown that CTGF/Hcs24 plays a major role in endochondral ossification.
Methods. Ossified ligament tissues were taken from seven male OPLL patients during surgery. Immunohistochemical staining was performed using an antibody specific for CTGF/Hcs24. Spinal ligament cells were isolated from five OPLL patients as well as five non-OPLL patients. The cells were incubated with recombinant human CTGF/Hcs24 or TGFbeta. The expression of ALP was analyzed by RT-PCR. For the effects of TGFbeta, the expression of CTGF/Hcs24 mRNA was analyzed.
Results. Immunohistochemical staining showed that chondrocytes in the transitional region from nonossified to ossified ligament were stained with an antibody against,,CTGF/Hcs24. It was found that CTGF/Hcs24 enhanced the expression ALP mRNA in OPLL cells, whereas the expression remained unchanged in non-OPLL cells. The-expression of CTGF/Hcs24 mRNA in OPLL and non-OPLL cell lines was increased by TGFbeta, and there was no significant difference between the two groups. However, TGFbeta and CTGF/Hcs24 enhanced the expression of ALP mRNA only in OPLL cells.
Conclusions. According to the study results, CTGF/Hcs24 may not only be an important factor in the development of endochondral ossification in OPLL, but may also be responsible for initiating osteogenesis in spinal ligament cells.

DOI： 10.1097/01.BRS.0000025725.06173.C6

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ヒト口腔扁平上皮癌細胞株における結合組織成長因子(CTGF)の腫瘍細胞増殖抑制効果

森谷徳文, 久保田聡, 近藤誠二, 西田崇, 川木晴美, 菅原利夫, 滝川正春

歯科基礎医学会雑誌 44 ( 5 ) 395 - 395 2002.9

Suppression of urokinase receptor expression by bikunin is associated with inhibition of upstream targets of extracellular signal-regulated kinase-dependent cascade

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

EUROPEAN JOURNAL OF BIOCHEMISTRY 269 ( 16 ) 3945 - 3957 2002.8

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

Our laboratory showed that bikunin, a Kunitz-type protease inhibitor, suppresses 4beta-phorbol 12-myristate 13-acetate (PMA)- or tumor necrosis factor-alpha (TNFalpha)-induced urokinase-type plasminogen activator (uPA) expression in different cell types. In addition to its effects on protease inhibition, bikunin could be modulating other cellular events associated with the metastatic cascade. To test this hypothesis, we examined whether bikunin was able to suppress the expression of uPA receptor (uPAR) mRNA and protein in a human chondrosarcoma cell line, HCS-2/8, and two human ovarian cancer cell lines, HOC-1 and HRA. The present study showed that (a) bikunin suppresses the expression of constitutive and PMA-induced uPAR mRNA and protein in a variety of cell types; (b) an extracellular signal-regulated kinase (ERK) activation system is necessary for the PMA-induced increase in uPAR expression, as PD098059 and U0126, which prevent the activation of MEK1, reduce the uPAR expression; (c) bikunin markedly suppresses PMA-induced phosphorylation of ERK1/2 at the concentration that prevents uPAR expression, but does not reduce total ERK1/2 antigen level; (d) bikunin has no ability to inhibit overexpression of uPAR in cells treated with sodium vanadate; and (e) we further studied the inhibition of uPAR expression by stable transfection of HRA cells with bikunin gene, demonstrating that bikunin secretion is necessary for inhibition of uPAR expression. We conclude that bikunin downregulates constitutive and PMA-stimulated uPAR mRNA and protein possibly through suppression of upstream targets of the ERK-dependent cascade, independent of whether cells were treated with exogenous bikunin or transfected with bikunin gene.

DOI： 10.1046/j.1432-1033.2002.03068.x

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CD44 stimulation by fragmented hyaluronic acid induces upregulation and tyrosine phosphorylation of c-Met receptor protein in human chondrosarcoma cells

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

BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH 1591 ( 1-3 ) 37 - 44 2002.8

Language：English Publishing type：Research paper (scientific journal) Publisher：ELSEVIER SCIENCE BV

Hepatocyte growth factor/scatter factor (HGF/SF) can induce proliferation and motility and promote invasion of tumor cells. Since HGF/SF receptor, c-Met, is expressed by tumor cells, and since stimulation of CD44, a transmembrane glycoprotein known to bind hyaluronic acid (HA) in its extracellular domain, is involved in activation of c-Met, we have studied the effects of CD44 stimulation by ligation with HA upon the expression and tyrosine phosphorylation of c-Met on human chondrosarcoma cell line HCS-2/8. The current study indicates that (a) CD44 stimulation by fragmented HA upregulates expression of c-Met proteins; (b) fragmented HA also induces tyrosine phosphorylation of c-Met protein within 30 min, an early event in this pathway as shown by the early time course of stimulation; (c) the effects of HA fragments are critically HA size-dependent. High molecular weight HA is inactive, but lower molecular weight fragments (M(r) 3.5 kDa) are active with maximal effect in the mug/ml range; (d) the standard form of CD44 (CD44s) is critical for the response because the effect on c-Met, both in terms of upregulation and phosphorylation, is inhibited by preincubation with an anti-CD44 monoclonal antibody; and (e) phosphorylation of c-Met induced by CD44 stimulation is inhibited by protein tyrosine kinase inhibitor, tyrphostin. Therefore, our study represents the first report that CD44 stimulation induced by fragmented HA enhances c-Met expression and tyrosine phosphorylation in human chondrosarcoma cells. Taken together, these studies establish a signal transduction cascade or cross-talk emanating from CD44 to c-Met. (C) 2002 Elsevier Science B.V. All rights reserved.

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cDNA array reveals mechanosensitive genes in chondrocytic cells under hydrostatic pressure

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

BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH 1591 ( 1-3 ) 45 - 54 2002.8

Language：English Publishing type：Research paper (scientific journal) Publisher：ELSEVIER SCIENCE BV

Hydrostatic pressure (HP) has a profound effect on cartilage metabolism in normal and pathological conditions, especially in weight-bearing areas of the skeletal system. As an important component of overall load, HP has been shown to affect the synthetic capacity and wellbeing of chondrocytes, depending on the mode, duration and magnitude of pressure. In this study we examined the effect of continuous HP on the gene expression profile of a chondrocytic cell line (HCS-2/8) using a cDNA array containing 588 well-characterized human genes under tight transcriptional control. A total of 51 affected genes were identified, many of them not previously associated with mechanical stimuli. Among the significantly up-regulated genes were immediate-early genes, and genes involved in heat-shock response (hsp70, hsp40, hsp27), and in growth arrest (GADD45, GADD153, p21(Cip1/Waf1), tob). Markedly down-regulated genes included members of the Id family genes (dominant negative regulators of basic helix-loop-helix transcription factors), and cytoplasmic dynein light chain and apoptosis-related gene NIP3. These alterations in the expression profile induce a transient heat-shock gene response and activation of genes involved in growth arrest and cellular adaptation and/or differentiation. (C) 2002 Elsevier Science B.V. All rights reserved.

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軟骨由来成長因子CTGF/Hcs24の細胞種特異的遺伝子発現抑制機構の解析

森谷徳文, 久保田聡, 江口傑徳, 近藤誠二, 菅原利夫, 滝川正春

生化学 74 ( 8 ) 913 - 913 2002.8

結合組織成長因子CTGF/Hcs24は細胞内で細胞骨格蛋白質と結合する

吉道玄, 久保田聡, 服部高子, 西田崇, 縄稚久美子, 中西徹, 山本照子, 滝川正春

生化学 74 ( 8 ) 797 - 797 2002.8

CTGF/Hcs24, a hypertrophic chondrocyte-specific gene product, stimulates proliferation and differentiation, but not hypertrophy of cultured articular chondrocytes Reviewed

T Nishida, S Kubota, T Nakanishi, T Kuboki, G Yosimichi, S Kondo, M Takigawa

JOURNAL OF CELLULAR PHYSIOLOGY 192 ( 1 ) 55 - 63 2002.7

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

We previously reported that connective tissue growth factor/hypertrophic chondrocyte-specific gene product 24 (CTCF/Hcs24) stimulated the proliferation and differentiation of rabbit growth cartilage (RGC) cells in vitro. In this study, we investigated the effects of CTGF/Hcs24 on the proliferation and differentiation of rabbit articular cartilage (RAC) cells in vitro. RAC cells transduced by recombinant adenoviruses generating mRNA for CTGF/Hcs24 synthesized more proteoglycan than the control cells. Also, treatment of RAC cells with recombinant CTGF/Hcs24 (rCTGF/Hcs24) increased DNA and proteoglycan syntheses in a dose-dependent manner. Northern blot analysis revealed that the rCTGF/Hcs24 stimulated the gene expression of type II collagen and aggrecan core protein, which are markers of chondrocyte maturation, in both RGC and RAC cells. However, the gene expression of type X collagen, a marker of hypertrophic chondrocytes, was stimulated by rCTGF/Hcs24 only in RGC cells, but not in RAC cells. Oppositely, gene expression of tenascin-C, a marker of articular chondrocytes, was stimulated by rCTGF/Hcs24 in RAC cells, but not in RGC cells. Moreover, rCTGF/Hcs24 effectively increased both alkaline phosphatase (ALPase) activity and matrix calcification of RGC cells, but not of RAC cells. These results indicate that CTGF/Hcs24 promotes the proliferation and differentiation of articular chondrocytes, but does not promote their hypertrophy or calcification. Taken together, the data show that CTCF/Hcs24 is a direct growth and differentiation factor for articular cartilage, and suggest that it may be useful for the repair of articular cartilage. (C) 2002 Wiley-Liss, Inc.

DOI： 10.1002/jcp.10113

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Autoimmunity against YKL-39, a human cartilage derived protein, in patients with osteoarthritis

JI Tsuruha, K Masuko-Hongo, T Kato, M Sakata, H Nakamura, T Sekine, M Takigawa, K Nishioka

JOURNAL OF RHEUMATOLOGY 29 ( 7 ) 1459 - 1466 2002.7

Language：English Publishing type：Research paper (scientific journal) Publisher：J RHEUMATOL PUBL CO

Objective. Our previous study revealed that some patients with rheumatoid arthritis (RA) possessed autoantibodies to YKL-39, a cartilage related protein. We investigated whether patients with osteoarthritis (OA) also displayed autoimmunity to YKL-39.
Methods. Autoantibodies to recombinant YKL-39 as well as human cartilage glycoprotein-39 were detected by ELISA and Western blotting. The tested serum samples were derived from 117 patients with OA, 94 patients with RA, and 2 groups of 50 arthropathy-free healthy donors who matched the OA and RA groups for age and sex. We determined autoepitopes on YKL-39 using 3 overlapping fragments of YKL-39 (designated F1, F2, F3). T cell proliferation response to YKL-39 was analyzed using the H-3-thymidine incorporation assay.
Results. Autoantibodies to YKL-39 were detected in 13 (11.1%) patients with OA and 11 (11.8%) with RA. In the epitope mapping, all the 3 fragments of YKL-39 were found to carry autoepitopes, but F1 was recognized most frequently. Proliferative responses of peripheral blood mononuclear cells against YKL-39 were detected in 6 (46%) of the 13 OA patients who were positive for the anti-YKL-39 autoantibodies and in 2 (17%) of the 11 antibody positive RA patients.
Conclusion. These results show that autoimmunity to YKL-39 in patients with OA was present at equal or somewhat higher frequency than in patients with RA. The cellular and humoral immune responses to YKL-39 may be involved in the pathological process of OA as well as RA.

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A novel cis-element that enhances connective tissue growth factor gene expression in chondrocytic cells

T Eguchi, S Kubota, S Kondo, T Kuboki, H Yatani, M Takigawa

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 295 ( 2 ) 445 - 451 2002.7

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

To clarify the chondrocyte-specific regulatory mechanism of connective tissue growth factor (ctgf) gene expression, we analyzed the functionality and DNA-protein interaction of the CTGF promoter. Comparative luciferase assay of the CTGF promoter deletion mutants among HCS-2/8 chondrocytic cells and fibroblastic cells revealed that a 110-bp region in the promoter was crucial for the HCS-2/8-specific transcriptional enhancement. Subsequent competitive gel shift assay revealed that transcription factors in HCS-2/8 nuclei bound to a 60-bp portion in the corresponding region. Relative luciferase activity from a CTGF promoter with mutant TGF-beta response element (TbRE) was 16.9% lower than that from an intact promoter. On the other hand, relative luciferase activity from a CTGF promoter with 4 bp point mutations at 30 bp upstream of the TbRE was 47.7% lower than that from the intact one. The binding activity of HCS-2/8 nuclear factor(s) to the sequence over the 4-bp was remarkably higher than that of any nuclear extract from other types of cells. Therefore, we entitled the sequence 'TRENDIC', a transcription enhancer dominant in chondrocytes, which stands for a novel enhancer for chondrocyte-specific CTGF gene expression. (C) 2002 Elsevier Science (USA). All rights reserved.

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結合組織成長因子(CTGF)の構造・機能解析のためのELISAシステムの開発

川木晴美, 久保田聡, 湊雅直, 森谷徳文, 服部高子, 大山和美, 中西徹, 滝川正春

岡山歯学会雑誌 21 ( 1 ) 182 - 183 2002.6

YKL-39, a human cartilage-related protein, induces arthritis in mice

M Sakata, K Masuko-Hongo, J Tsuruha, T Sekine, H Nakamura, M Takigawa, K Nishioka, T Kato

CLINICAL AND EXPERIMENTAL RHEUMATOLOGY 20 ( 3 ) 343 - 350 2002.5

Language：English Publishing type：Research paper (scientific journal) Publisher：CLINICAL & EXPER RHEUMATOLOGY

Objective
To determine whether YKL-39, a recently cloned secretory protein of articular chondrocytes, is arthritogenic in mice. Methods Recombinant YKL-39 (rYKL-39) was expressed and purified from E. coli. To induce arthritis in mice, rYKL-39 (1, 10 or 50 mug in Freund's incomplete adjuvant) was injected into the right footpad of mice from four different strains (BALB/c, DBA/1J, C57BL/6 and ICR). The mice received a second immunization with rYKL-39 by intradermal injection into the root of the tail 10 days after the first immunization. Severin, of arthritis was assessed by scoring each paw on a scale from 0 to 4. Sixty days after the first immunization, the mice were sacrificed and the joints were examined by immunohistochemistry and radiography. The anti-YKL-39 and anti type II-collagen (CII) antibody titres were also assayed using ELISA.
Results
Immunization with YKL-39 induced arthritis in all strains of mice tested, among which BALB/c was most susceptible. Histological examination showed synovial proliferation and irregularity of the cartilage surface in YKL-39-injected BALB/c mice. Moreover radiographic analysis revealed pathological changes in these mice. The YKL-39-immunised mice produced not only anti-YKL-39 antibody but also antibody against AN H collagen, suggesting a spreading of autoimmunity after YKL-39.
Conclusions
YKL-39, a cartilage-related protein, is found to induce arthritis accompanied by pathologic changes in bone and cartilage. A better understanding of the immune response against cartilage-related components including YKL-39 may help to elucidate the pathological processes of arthritic disorders.

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Connective tissue growth factor increased by hypoxia may initiate angiogenesis in collaboration with matrix metalloproteinases

S Kondo, S Kubota, T Shimo, T Nishida, G Yosimichi, T Eguchi, T Sugahara, M Takigawa

CARCINOGENESIS 23 ( 5 ) 769 - 776 2002.5

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

Connective tissue growth factor (CTGF) is known to be a potent angiogenic factor. Here we investigated how CTGF and matrix metalloproteinases (MMPs) are involved in the early stage of hypoxia-induced angiogenesis using human breast cancer cell line, MDA231, and vascular endothelial cells. Hypoxic stimulation (5% O-2) of MDA231 cells increased their steady-state level of ctgf mRNA by similar to2-fold within 1.5 h, and the levels remained at a plateau up to 6 h, and then decreased by 12 h as compared with the cells cultured under the normoxic condition. Membrane-type 1 MMP (MT1-MMP) mRNA levels was also increased within a few hours of the exposure to hypoxia. Indeed, ELISA revealed that the CTGF protein/cell in medium conditioned by MDA231 cells exposed to hypoxia was maximally greater at 24 h than in the medium from normoxic cultures and that the secretion rate (supernatant CTGF/cell layer CTGF) increased in a time-dependent manner from 24 to 72 h of hypoxic exposure. Hypoxic induction of CTGF was also confirmed by immunohistochemical analyses. Furthermore, zymogram analysis revealed that the production of active MMP-9 was also induced in MDA231 cells incubated under hypoxic conditions. Finally, we found that recombinant CTGF also increased the expression of a number of metalloproteinases that play a role in the vascular invasive processes and decreased the expression of tissue inhibitors of metalloproteinases by vascular endothelial cells. These findings suggest that hypoxia stimulates MDA231 cells to release CTGF as an angiogenic modulator, which initiates the invasive angiogenesis cascade by modulating the balance of extracellular matrix synthesis and degradation via MMPs secreted by endothelial cells in response to CTGF. This cascade may play critical roles in the hypoxia-induced neovascularization that accompanies tumor invasion in vivo.

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軟骨由来軟骨成長因子(CTGF/Hcs24)を用いた関節軟骨再生療法の検討

小島俊司, 西田崇, 小森千尋, 藤沢拓生, 窪木拓男, 矢谷博文, 中西徹, 滝川正春

日本顎関節学会雑誌 14 ( 1 ) 81 - 81 2002.4

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