Faculty Profiles - HATTORI Takako

Papers - HATTORI Takako

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A highly conserved enhancer in mammalian type X collagen genes drives high levels of tissue-specific expression in hypertrophic cartilage in vitro and in vivo. Reviewed International journal

Sonja Gebhard, Ernst Pöschl, Silvia Riemer, Eva Bauer, Takako Hattori, Heidi Eberspaecher, Zhaoping Zhang, Veronique Lefebvre, Benoit de Crombrugghe, Klaus von der Mark

Matrix biology : journal of the International Society for Matrix Biology 23 ( 5 ) 309 - 22 2004.8

Language：English Publishing type：Research paper (scientific journal)

Previously we have identified a cis-acting regulatory domain in the human type X collagen gene upstream of the transcription start site which acts as a strong enhancer in hypertrophic, but not in resting chondrocytes. Here we show that this enhancer is highly conserved also in the murine and bovine Col10a1 genes, but not found in the known promoter sequences of chicken Col10a1. It contains a functionally active AP-1 site (TPA Responsive Element, TRE) which is essential for the high transcriptional activity of the COL10A1 enhancer in transiently transfected hypertrophic chondrocytes. Gel-shift experiments with nuclear extracts of hypertrophic chondrocytes revealed FosB and Fra-1 as candidates regulating AP-1 factors binding to the TRE site. In fact, coexpression of FosB and Fra-1 in reporter gene assays greatly stimulated transcriptional activity of enhancer bearing reporter genes. Quantitative analysis of AP-1 factor mRNA levels in distinct fractions of fetal bovine epiphyseal chondrocytes by real-time PCR confirmed significant levels of FosB and Fra-1 mRNA besides other AP-1 factors in hypertrophic chondrocytes. A key role of the enhancer element in regulating tissue-specific expression of the Col10a1 gene was shown by establishing transgenic mouse lines with a reporter gene containing a 4.6 kb murine Col10a1 promoter fragment which included the enhancer, exon 1, part of exon 2 and the first intron. Reporter gene expression was seen exclusively in hypertrophic cartilages in the growth plates of long bones, ribs, vertebrae, sternum and mandibles of 17.5-18.5 dpc embryos, confirming that the 4.6 kb promoter is able to drive specific expression of Col10a1 in hypertrophic cartilage. These established transgenic lines should facilitate the genetic analysis of regulatory pathways of chondrocyte maturation and Col10a1 gene expression in the future.

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Novel enzyme-linked immunosorbent assay systems for the quantitative analysis of connective tissue growth factor (CTGF/Hcs24/CCN2): Detection of HTLV-I tax-induced CTGF from a human carcinoma cell line Reviewed International journal

H Kawaki, S Kubota, M Minato, NH Moritani, T Hattori, H Hanagata, M Kubota, A Miyauchi, T Nakanishi, M Takigawa

DNA AND CELL BIOLOGY 22 ( 10 ) 641 - 648 2003.10

Language：English Publishing type：Research paper (scientific journal) Publisher：MARY ANN LIEBERT INC PUBL

Connective tissue growth factor/hypertrophic chondrocyte-specific gene product 24 (CTGF/Hcs24/CCN2) is known as a multifunctional growth factor. It stimulates proliferation, migration, and extracellular matrix production of mesenchymal cells, and is highly expressed in hypertrophic chondrocytes. In this study, we constructed useful ELISA systems for the analysis of CTGF and its modular fragments. For this objective we prepared four different antihuman CTGF monoclonal antibodies. One, specific for the VWC module, was utilized as the detecting antibody, and the other three, recognizing CT, IGFBP, and VWC modules, respectively, were employed as capture antibodies. Then we established three novel quantitative analysis systems for CTGF. The first system recognizing CT and VWC modules was useful to measure full-length CTGF with improved sensitivity. Utilizing this system, we found significant enhancement of CTGF production from a human carcinoma cell line transduced by HTLV-I tax gene, where the finding indicates the possible involvement of Tax in carcinogenesis. The second system, seeing IGFBP and VWC modules, could quantify not only CTGF, but also may be useful to analyze processed N-terminal fragments. The third system, utilizing capture and detection antibodies against the VWC module, was able to quantify the VWC module only, while it did not recognize full-length CTGF. Since CTGF is actually processed into subfragments, and functional assignment of each module is of interest, these systems are expected to contribute to the progress of CTGF investigations.

DOI： 10.1089/104454903770238111

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

Takako Hattori, Harumi Kawaki, Satoshi Kubota, Yasutaka Yutani, Benoit de Crombrugghe, Klaus von der Mark, Masaharu Takigawa

Journal of cellular physiology 197 ( 1 ) 94 - 102 2003.10

Authorship：Lead author Language：English Publishing type：Research paper (scientific journal)

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 downregulation 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 downregulation 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.

DOI： 10.1002/jcp.10341

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

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.

DOI： 10.1177/154405910308200914

CTGF/Hcs24 interacts with the cytoskeletal protein actin in chondrocytes Reviewed International journal

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.

DOI： 10.1016/s0006-291x(02)02739-0

[Articular cartilage regeneration].

Takako Hattori, Shigeyuki Wakitani

Clinical calcium 12 ( 2 ) 217 - 21 2002.2

Language：Japanese Publishing type：Research paper (scientific journal)

The main functions of articular cartilages are load-bearing and reducing friction of the articular surfaces. Because the capacity of articular cartilage to repair is limited, many attempts have been made to repair articular cartilage defects, which include transplantations of various tissues or cells. Within them, autologous cultured chondrocyte or autologous bone marrow mesenchymal cell transplantations are reported to be useful methods to repair articular cartilage defects. Here, we introduce these methods of tissue engineering and gene therapy, which are expected to become new treatments of articular cartilage defects.

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CTGF/Hcs24 induces chondrocyte differentiation through a p38 mitogen-activated protein kinase (p38MAPK), and proliferation through a p44/42 MAPK/extracellular-signal regulated kinase (ERK) Reviewed

G Yosimichi, T Nakanishi, T Nishida, T Hattori, T Takano-Yamamoto, M Takigawa

EUROPEAN JOURNAL OF BIOCHEMISTRY 268 ( 23 ) 6058 - 6065 2001.12

Language：English Publishing type：Research paper (scientific journal) Publisher：BLACKWELL SCIENCE LTD

Connective tissue growth factor/hypertrophic chondrocyte specific gene product 24 (CTGF/Hcs24) promotes proliferation and differentiation of chondrocytes in culture. We investigated the roles of two major types of mitogen activated protein kinase (MAPK) in the promotion of proliferation and differentiation by CTGF/Hcs24. Here we report the effects of the MAPKK/MEK 1/2 inhibitor, PD098059, and p38 MAPK inhibitor, SB203580, in a human chondrosarcoma-derived chondrocytic cell line (HCS-2/8) and rabbit growth cartilage (RGC) cells treated with CTGF/Hcs24. In the proliferation phase, CTGF/Hcs24 induced a approximate to fivefold increase in the phosphorylation of p44/42 MAPK/ERK and a approximate to twofold increase in that of p38 MAPK in an in vivo kinase assay. These inhibitors of MAPKK and MAPK suppressed phosphorylation of ets-like gene-1 (Elk-1) and nuclear activating transcription factor-2 (Atf-2) induced by CTGF/Hcs24 in a dose-dependent manner, respectively. Western blot analysis showed that phosphorylation of ERK was induced from 30 to 60 min and phosphorylation of p38 MAPK from 10 to 15 min after the addition of CTGF/Hcs24 in confluence HCS-2/8 cells. PD098059 suppressed the DNA synthesis of HCS-2/8 cells and RGC cells, while SB203580 did not. On the other hand, the p38 MAPK inhibitor, SB203580, completely inhibited the CTGF/Hcs24-induced synthesis of proteoglycans in HCS-2/8 cells and RGC cells but the MEK1/2 inhibitor, PD098059, did not. These results suggest that ERK mediates the CTGF/Hcs24-induced proliferation of chondrocytes, and that p38 MAPK mediates the CTGF/Hcs24-induced differentiation of chondrocytes.

DOI： 10.1046/j.0014-2956.2001.02553.x

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Cell-type-specific trans-activation of herpes simplex virus thymidine kinase promoter by the human T-cell leukemia virus type I Tax protein. Reviewed

Kubota S, Mukudai Y, Hattori T, Eguchi T, Kondo S, Takigawa M

DNA and cell biology 20 ( 9 ) 563 - 568 2001.9

Change in cellular localization of a rheumatoid arthritis-related antigen (RA-A47) with downregulation upon stimulation by inflammatory cytokines in chondrocytes. Reviewed

Hattori, T, Kubota, S, Yutani Y, Fujisawa T, Nakanishi, T, Takahashi, K, Takigawa M

J. Cell. Physiol. 186 268 - 281 2001

Regulatory mechanism of human connective tissue growth factor (CTGF/Hcs24) gene expression in a human chondrocytic cell line, HCS-2/8. Reviewed

Eguchi, T, Kubota, S, Kondo, S, Shimo, T, Hattori, T, Nakanishi, T, Kuboki, T, Yatani, H, Takigawa, M

J. Biochem. 130 79 - 87 2001

Novel mode of processing and secretion of connective tissue growth factor/ecogenin (CTGF/Hcs24) in chondrocytic HCS-2/8 cells. Reviewed

Kubota, S, Eguchi, T, Shimo, T, Nishida T, Hattori, T, Kondo, S, Nakanishi, T, Takigawa, M

Bone 29 155 - 161 2001

Characterization of a Mouse ctgf 3′-UTR Segment That Mediates Repressive Regulation of Gene Expression Reviewed

Seiji Kondo, Satoshi Kubota, Takanori Eguchi, Takako Hattori, Tohru Nakanishi, Toshio Sugahara, Masaharu Takigawa

Biochemical and Biophysical Research Communications 278 ( 1 ) 119 - 124 2000.11

Publishing type：Research paper (scientific journal) Publisher：Elsevier BV

We isolated a small segment of the 3'-untranslated region (3'-UTR) in the mouse connective tissue growth factor (ctgf/fisp12) gene and evaluated its functionality. Comparison of the nucleotide sequences of human and mouse ctgf 3'-UTRs revealed a conserved small segment of 91 bases. The corresponding segments of the 3'-UTRs shared as much as 82.4% homology, whereas the overall homology between the 3'-UTRs was 71.8%. To study the functionality of the conserved segment, the corresponding region of mouse ctgf cDNA was amplified from NIH3T3 cells. When it was fused downstream of a marker gene, it showed remarkable repressive effects on gene expression. The repressive effect of the sense form was more prominent than that of the antisense form. Computer analyses of these sequence predicted stable secondary structures, suggesting that they act at the RNA level. The predicted structures of the sense and antisense forms appeared to be slightly different, which is consistent with the difference in repressive function. These findings defined the conserved small element in the mouse ctgf gene as a potent negative regulator of gene expression, which may act at a posttranscriptional level. (C) 2000 Academic Press.

DOI： 10.1006/bbrc.2000.3780

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Shear bond strengths of orthodontic plastic brackets

G. Guan, T. Takano-Yamamoto, M. Miyamoto, T. Hattori, K. Ishikawa, K. Suzuki

American journal of orthodontics and dentofacial orthopedics : official publication of the American Association of Orthodontists, its constituent societies, and the American Board of Orthodontics 117 ( 4 ) 438 - 443 2000.4

Publishing type：Research paper (scientific journal)

The purpose of the present study was to evaluate the shear bond strengths of plastic brackets and the influences of the bracket filler contents on the bonding. The shear bond strengths of 4 plastic brackets (Spirit; Spirit MB; Clear Bracket; Aesthetic-Line) bonded to enamel with 4 orthodontic adhesives (Orthomite Superbond; System 1+; Transbond XT; and Kurasper-F) were compared with the strength of a conventional metal bracket. The findings of this study indicated the following: (1) shear bond strength of the 4 plastic brackets was significantly lower than that of the conventional metal brackets (P <.05), with most of the values ranging from 3 MPa to 6 MPa; (2) when comparing the bond strengths of plastic brackets, Aesthetic-Line had the largest value followed by Spirit MB, Spirit, and Clear Bracket, and when the plastic brackets were bonded with Orthomite Superbond, they showed relatively stronger bond strengths than when bonded with the other adhesives. Clear Bracket showed relatively lower values especially when bonded with System 1+; (3) the application of primer did not increase the durability of the bond strengths when bonding Spirit and Clear brackets; and (4) fillers contained in each plastic bracket ranging from 9.18% to 19. 52% were fairly well distributed and showed the same morphology of a fiber type 10 microm in diameter with different lengths. The filler concentration tended to correlate with the bond strength. The exposed fillers on the bracket base surface may play a more important role in plastic bracket adhesion than the macro-morphology of the base surface.

DOI： 10.1016/S0889-5406(00)70163-6

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Matrix Metalloproteinases and Tissue Inhibitors of Metalloproteinases in Synovial Fluids of Patients with Temporomandibular Joint Osteoarthritis Reviewed

Manabu Kanyama, Takuo Kuboki, Shunji Kojima, Takuo Fujisawa, Takako Hattori, Masaharu Takigawa, Atsushi Yamashita

Journal of Orofacial Pain 14 ( 1 ) 20 - 30 2000

Language：English Publishing type：Research paper (scientific journal)

Aims: Imbalance between matrix metalloproteinases (MMPs) and their inhibitors (TIMPs) may be involved in the breakdown of articular cartilage matrix of the temporomandibular joint (TMJ). Aims: In this study, MMPs, TIMPs, and MMP-1/TIMP-1 complex levels were examined in TMJ synovial fluid samples aspirated from TMJ osteoarthritis (OA) patients (2 males, 8 females
mean age, 29.7 years) and asymptomatic control subjects (2 males, 8 females
mean age, 23.6 years) to determine the likelihood of increased proteolytic activity in the OA joints. Methods: The various types of MMPs and TIMPs were detected by Western blotting with monoclonal antibodies and gelatin zymography. The MMP-1/ TIMP-1 complex level was measured by an enzyme-linked immunosorbent assay kit. All aspirates were first analyzed for total protein content and then individually diluted to make the total protein levels equivalent. Results: The mean MMP-1/TIMP-1 complex concentration in the synovial fluids of the OA patients was 3.92 ± 1.39 ng/mL
this value was significantly lower (P &lt
0.05) than the value from control subjects (5.46 ± 1.32 ng/mL). Matrix metalloproteinase-1 (52 kDa), MMP-3 (57 kDa), TIMP-1 (28 kDa), and TIMP-2 (26 kDa) were detected in all of the normal and the OA samples. However, MMP-1 (28 kDa), MMP-2 (72 kDa), MMP-3 (45 kDa), and MMP-9 (83 kDa) were detected in higher concentration in the OA samples. Conclusion: These findings suggest a strong association between the OA-active joints and the presence of biologically active forms of known tissue degradation enzymes (MMP-1, MMP-3, and MMP-9).

Novel intracellular effects of human connective tissue growth factor expressed in Cos-7 cells.

Kubota, S, Hattori, T, Shimo, T, Nakanishi, T, Takigawa, M

FEBS Letters 474 58 - 62 2000

Identification of an RNA element that confers post-transcriptional repression of connective tissue growth factor/hypertrophic chondrocyte specific 24 (ctgf/hcs24) gene: Similarities to retroviral RNA-protein interactions. Reviewed

Kubota, S, Kondo, S, Eguchi1, T, Hattori, T, Nakanishi, T, Pomerantz, R.J, Takigawa, M

Oncogene 19 4773 - 4786 2000

軟骨由来の慢性関節リウマチ関連抗原RA-A47に関する研究（Study on a rheumatoid arthritis-related antigen (RA-A47) isolated from chondrocytes）. Reviewed

服部高子

2000

Rheumatoid arthritis-related antigen 47kDa (RA-A47) is a product of colligin-2 and acts as a human HSP47 Reviewed

T Hattori, K Takahashi, Y Yutani, T Fujisawa, T Nakanishi, M Takigawa

JOURNAL OF BONE AND MINERAL METABOLISM 18 ( 印刷中 ) 323 - 334 2000

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

We previously isolated RA-A47, which is recognized as an antigen of rheumatoid arthritis (RA), from a human chondrosarcoma-derived cell line (HCS-2/8). The N-terminal 21-amino-acid sequence of RA-A47 had 81% homology to the deduced amino acid sequence of the human heat-shock protein (HSP) 47 gene, the colligin gene, and 100% homology to that of the colligin-2 gene. Moreover, as is HSP47, RA-A47 was a heat-inducible collagen-binding protein. To further characterize RA-A47, we isolated ra-a47 cDNA from HCS-2/8 cells and human periodontal ligament fibroblast (HPLF) cells. The isolated ra-a47 cDNAs from both cells were almost the same as that of collipin-2. C-504 and G(505) in the cDNA sequences of both cells and C-598 in the cDNA of HCS-2/8 were different from the corresponding bases of colligin-2 cDNA. These differences were also observed in genomic DNA. colligin cDNA was not isolated. To show that the isolated cDNA encodes RA-A47 protein, it was expressed in Cos-7 cells. The produced protein was 47 kDa and was recognized both with RA sera and antirat HSP47 antibody, indicating that it is RA-A47 and has structural similarity to HSP47. These results taken together with our previous finding show that RA-A47 is the putative colligin-2 gene product and behaves as a human HSP47. Although colligin has been considered the human HSP47 gene, failure to detect the colligin gene and its mRNA suggests that colligin does not exist in human cells and that the HSP47 gene is identical with colligin-2, which encodes RA-A47.

DOI： 10.1007/s007740070004

Other Link： https://search.jamas.or.jp/index.php?module=Default&action=Link&pub_year=2000&ichushi_jid=J04654&link_issn=&doc_id=20001102080004&doc_link_id=10.1007%2Fs007740070004&url=https%3A%2F%2Fdoi.org%2F10.1007%2Fs007740070004&type=Crossref&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00002_2.gif

軟骨細胞様培養細胞株HCS-2/8における慢性関節リウマチ関連抗原RA-A47の炎症性サイトカインによる発現抑制と細胞内局在変化. (Downregulation of a rheumatoid arthritis-related antigen (RA-A47) by stimulation of inflammatory cytokines in chondrocytic cell line, HCS-2/8). Reviewed

服部高子

岡山歯学会雑誌 19 ( 2 ) 241 - 254 2000

Authorship：Lead author,　Corresponding author Language：Japanese Publisher：岡山歯学会

ra-a47mRNAにおいてTGFβで発現量が増加し,II型コラーゲン遺伝子(COL2A1)mRNAの発現量の増加と同調していることが観察された.対称的に,腫瘍壊死因子(TNF)α,インターフェロン(IFN)β,インターロイキン(IL)-6等の炎症性サイトカイン刺激によってra-a47mRNAの発現量は減少したが,COL2A1mRNAの発現量は減少せず,むしろ増加することがHCS-2/8で観察された.更に,誘導型一酸化窒素合成酵素(iNOS)mRNA,マトリックスメタロプロテアーゼ(MMP-9)mRNAの発現がTNFα刺激で強く誘導されていることが明らかとなった

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Detection of specific antibodies against human cultured chondrosarcoma (HCS-2/8) and osteosarcoma (Saos-2) cells in the serum of patients with osteoarthritis of the temporomandibular joint Reviewed

T Kuboki, T Hattori, T Mizushima, M Kanyama, T Fujisawa, A Yamashita, M Takigawa

ARCHIVES OF ORAL BIOLOGY 44 ( 5 ) 403 - 414 1999.5

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

To find specific humoral antibodies in sera from patients with temporomandibular joint (TMJ) osteoarthritis (OA), an immortal human chondrocyte (HCS-2/8) and osteoblast (Saos-2) cell line derived from a chondrosarcoma and an osteosarcoma, respectively, were used as source proteins of human antigens. Patients with chronically painful TMJ OA (n = 18) but no other joints symptoms were selected from a consecutive series of patients with temperomandibular disorders and sex-matched asymptomatic controls (n = 8) were also recruited. Cellular proteins of the HCS-2/8 and Saos-2 cells were subjected to Western blotting with the OA and control sera as probes. Band-recognition frequency and the peak optical density of the band were compared between groups by chi(2) and t-tests. OA sera recognized various bands for the chondrocytes, and one of these (47-kDa) was specific for the OA sera. In two OA patients whose treatment outcome was less favorable, the,reactivity against the 47-kDa protein was relatively high. In addition, the OA sera clearly cross-reacted with recombinant HSP47. Based on these findings, an autoimmune reaction against chondrocytes could be one of the exaggerating and/or perpetuating mechanisms in the pathophysiology of osteoarthritic TMJs, and the humoral antibody titre against the HSP47-like protein derived from the chondrocytes could be one of the possible markers for the prognosis of the joint pathology. (C) 1999 Elsevier Science Ltd. All rights reserved.

DOI： 10.1016/s0003-9969(99)00009-6

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Papers - HATTORI Takako