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临床骨科杂志 2006年第4期9卷 381-384页

作者：蒋雷生张自明蒋盛旦戴力扬上海交通大学医学院附属新华医院骨科上海200092

肥胖对机体健康的不良影响已得到越来越多的重视,但人们在研究和防治肥胖的同时,也发现肥胖对骨骼有保护作用:肥胖者很少患有骨质疏松症,髋部骨折的发生率也较低。体重或体重指数(BMI)与骨密度(BMD)的相关性已经得到公认,许多研究进一... 详细信息

肥胖对机体健康的不良影响已得到越来越多的重视,但人们在研究和防治肥胖的同时,也发现肥胖对骨骼有保护作用:肥胖者很少患有骨质疏松症,髋部骨折的发生率也较低。体重或体重指数(BMI)与骨密度(BMD)的相关性已经得到公认,许多研究进一步证明体重的重要组成部分——体脂量(body fat mass)与BMD呈正相关。雌激素含量降低是绝经后妇女骨质疏松症的主要原因,而肥胖者脂肪组织中雄激素转变成雌激素增多,体重增加时骨骼所受到的应力也增加。[第一段]

关键词：瘦素骨/代谢软骨/代谢骨质疏松骨关节炎

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大骨节病软骨基质代谢异常与硒的关系的探讨

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甘肃医药 1985年第2期 3-5页

作者：徐吉敏甘肃省地方病防治研究所

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SOX9 enhances aggrecan gene promoter/enhancer activity and is up-regulated by retinoic acid in a cartilage-derived cell line, TC6

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第15期275卷 10738-10744页

作者： Sekiya, I Tsuji, K Koopman, P Watanabe, H Yamada, Y Shinomiya, K Nifuji, A Noda, M Tokyo Med & Dent Univ Inst Med Res Dept Mol Pharmacol Chiyoda Ku Tokyo 1010062 Japan Tokyo Med & Dent Univ Dept Orthopaed Surg Tokyo 101 Japan Univ Queensland Ctr Cellular & Mol Biol Brisbane Qld 4072 Australia NIDCR Dev Biol Lab NIH Bethesda MD 20892 USA

SOX9 is a transcription factor that plays a key role in chondrogenesis, Aggrecan is one of the major structural components in cartilage;however, the molecular mechanism of aggrecan gene regulation has not yet been fully elucidated, TC6 is a clonal chondrocytic cell line derived from articular cartilage, The purpose of this study was to examine whether SOX9 modulates aggrecan gene expression and to further identify molecules that regulate Sox9 expression in TC6 cells. SOX9 overexpression in TC6 cells enhanced by similar to 3-fold the transcriptional activity of the AgCAT-8 construct containing S-kilobase (kb) promoter/first exon/first intron fragments of the aggrecan gene. SOX9 enhancement of aggrecan promoter activity was lost when we deleted a 4.5-kb fragment from the 3'-end of the 8-kb fragment corresponding to the region including the first intron, In TC6 cells, SOX9 enhanced the transcriptional activity of a reporter construct containing the Sry/Sox consensus sequence >10-fold. SOX9 enhancement of aggrecan gene promoter activity and SOX9 transactivation through the Sry/Sox consensus sequence were not observed in osteoblastic osteosarcoma cells (ROS17/2.8), indicating the dependence on the cellular background. Northern blot analysis indicated that TC6 cells constitutively express Sox9 mRNA at relatively low levels. To examine regulation of Sox9 gene expression, we investigated the effects of calciotropic hormones and cytokines, Among these, retinoic acid (RA) specifically enhanced Sox9 mRNA expression in TC6 cells. The basal levels of Sox9 expression and its enhancement by RA were observed similarly at both permissive (33 degrees C) and nonpermissive (39 degrees C) temperatures. Furthermore, RA treatment enhanced the transcriptional activity of a reporter construct containing the Sry/Sox consensus sequence in TC6 cells. Moreover, RA treatment also enhanced the transcriptional activity of another reporter construct containing the enhancer region of the type II pro

关键词：软骨蛋白聚糖类碱性磷酸酶/遗传学软骨/代谢细胞系增强子元件遗传学细胞外基质蛋白质类基因表达调控/药物作用高迁移率族蛋白质类/生理学外源凝集素类 C型启动区遗传蛋白聚糖类/遗传学 SOX9转录因子类转录因子/生理学转录遗传/药物作用维甲酸/药理学增量调节动物小鼠

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FcγRI up-regulation induced by local adenoviral-mediated interferon-γ production aggravates chondrocyte death during immune complex-mediated arthritis

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AMERICAN JOURNAL OF PATHOLOGY 2003年第2期163卷 743-752页

作者： Nabbe, KC van Lent, PL Holthuysen, AE Kolls, JK Verbeek, S van den Berg, WB Univ Nijmegen Med Ctr Dept Expt Rheumatol & Adv Therapeut Nijmegen Netherlands Leiden Univ Med Ctr Dept Human & Clin Genet Leiden Netherlands Louisiana State Univ Hlth Sci Ctr New Orleans LA 70112 USA

Using various FcgammaR-deficient mice, we have obtained suggestive evidence that FcgammaRI on macrophages is responsible for severe cartilage destruction during arthritis mediated by immune complexes (ICs). This role of FcgammaRI is pronounced in the presence of activated Th1 cells and a likely Th1 cell-derived cytokine mediating up-regulation of FcgammaRI expression is interferon (IFN)-gamma. We now investigated whether local overexpression of IFN-gamma using an adenoviral vector is able to elevate cartilage destruction during experimental immune complex-mediated arthritis (ICA) and to what extent this process is FcgammaRI-mediated. IFN-gamma overexpression during ICA had no significant effect on the total cell mass infiltrating the knee joint. However, a higher percentage of macrophages expressing markers for a proinflammatory phenotype was found and these macrophages were situated in close proximity of the cartilage surface. interestingly, cartilage destruction as studied by matrix metalloproteinase (MMP)-mediated proteoglycan damage (VDIPEN expression), chondrocyte death, and erosion was significantly increased. This effect of IFN-gamma was only found in the presence of ICs, as IFN-gamma overexpression during zymosan-induced arthritis, which is not IC-dependent, did not lead to severe cartilage destruction. These results imply a crucial role for ICs and the IgG-binding receptors in the aggravation of cartilage damage by IFN-gamma. Local overexpression of IFN-gamma induced increased FcgammaRI mRNA levels in synovium. To study whether this up-regulation of FcgammaRI mediates aggravation of cartilage destruction, ICA was raised in FcgammaRI(-/-) and their wild-type controls. IFN-gamma resulted in elevated VDIPEN expression, which was still present in FcgammaRI(-/-). Of great interest, chondrocyte death remained low in FcgammaRI(-/-). These results indicate that IFN-gamma overexpression deteriorates cartilage destruction in the presence of ICs and that FcgammaRI is

关键词：腺病毒科/遗传学腺病毒科/免疫学抗原抗体复合物关节炎实验性关节炎类风湿/免疫学关节炎类风湿/代谢关节炎类风湿/病理学软骨/代谢软骨/病理学细胞死亡软骨细胞/生理学遗传载体干扰素γ/遗传学干扰素γ/代谢膝关节/代谢膝关节/病理学巨噬细胞活化小鼠近交BALBC 小鼠近交C57BL 小鼠基因敲除寡肽类/代谢肽碎片/代谢 RNA 信使/遗传学 RNA 信使/代谢受体 IgG/遗传学受体 IgG/代谢滑膜/免疫学增量调节酵母多糖/毒性动物小鼠

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CYTOKINES AND GROWTH-FACTORS WHICH REGULATE BONE CELL-FUNCTION

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ACTA ASTRONAUTICA 1994年第C期33卷 131-136页

作者： SEINO, Y Department of Pediatrics Okayama University Medical School 2-5-1 Shikata-cho Okayama 700 Japan

Everybody knows that growth factors are most important in making bone. Hormones enhance bone formation from a long distance. Growth factors promote bone formation as an autocrine or paracrine factor in nearby bone. BMP-2 through BMP-8 are in the TGF-beta family. BMP makes bone by enchondral ossification. In bone, IGF-II is most abundant, second, TGF-beta, and third IGF-I. TGF-beta enhances bone formation mainly by intramembranous ossification in vivo. TGF-beta affects both cell proliferation and differentiation, however, TGF-beta mainly enhances bone formation by intramembranous ossification. Interestingly, TGF-beta is increased by estrogen(E2), androgen, vitamin D, TGF-beta and FGF. IGF-I and IGF-II also enhance bone formation. At present it remains unclear why IGF-I is more active in bone formation than IGF-II, although IGF-II is more abundant in bone compared to IGF-I. However, if only type I receptor signal transduction promotes bone formation, the strong activity of IGF-I in bone formation is understandable. GH, PTH and E2 promotes IGF-I production. Recent data suggest that hormones containing vitamin D or E2 enhance bone formation through growth factors. Therefore, growth factors are the key to clarifying the mechanism of bone formation.

关键词：骨形态发生蛋白质类/代谢骨形态发生蛋白质类/生理学骨和骨组织/细胞学骨和骨组织/代谢骨和骨组织/生理学软骨/细胞学软骨/代谢细胞培养的胰岛素样生长因子结合蛋白质3/代谢胰岛素样生长因子结合蛋白质3/生理学胰岛素样生长因子结合蛋白质类/生理学胰岛素样生长因子Ⅰ/生理学胰岛素样生长因子Ⅱ/生理学骨细胞/代谢骨细胞/生理学骨生成/生理学转化生长因子β/代谢转化生长因子β/生理学维生素D/生理学维生素E/生理学动物女(雌)性男(雄)性大鼠

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Interleukin 17 induces cartilage collagen breakdown: novel synergistic effects in combination with proinflammatory cytokines

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ANNALS OF THE RHEUMATIC DISEASES 2002年第8期61卷 704-713页

作者： Koshy, PJ Henderson, N Logan, C Life, PF Cawston, TE Rowan, AD Newcastle Univ Sch Med Sch Clin Med Sci Dept Rheumatol Newcastle Upon Tyne NE4 2HH Tyne & Wear England Glaxo Wellcome Res & Dev Ltd Stevenage SG1 2NY Herts England

Objective: To investigate whether interleukin 17 (IL17), derived specifically from T cells, can promote type II collagen release from cartilage. The ability of IL17 to synergise with other proinflammatory mediators to induce collagen release from cartilage, and what effect anti-inflammatory agents had on this process, was also assessed. Methods: IL17 alone, or in combination with IL1, IL6, oncostatin M (OSM), or tumour necrosis factor alpha (TNFalpha), was added to bovine nasal cartilage explant cultures. Proteoglycan and collagen release were determined. Collagenolytic activity was determined by bioassay. Chondroprotective effects of IL4, IL13, transforming growth factor beta1 (TGFbeta1) and insulin-like growth factor-1 (IGF1) were assessed by inclusion in the explant cultures. Results: IL1 7 alone stimulated a dose dependent release of proteoglycan and type 11 collagen from bovine nasal cartilage explants. Suboptimal doses of IL17 synergised potently with TNFalpha, IL1, OSM, and IL6 to promote collagen degradation. This collagen release was completely inhibited by tissue inhibitor of metalloproteinase-1 and BB-94 (a synthetic metalloproteinase inhibitor), and was significantly reduced by IL4, IL13, TGFbeta1, and IGF1. In IL17 treated chondrocytes, mRNA expression for matrix metalloproteinase (MMP)-1, MMP-3, and MMP-13 was detected. Moreover, a synergistic induction of these MMPs was seen when IL17 was combined with other proinflammatory cytokines. Conclusions: IL17 can, alone and synergistically in combination with other proinflammatory cytokines, promote chondrocyte mediated MMP dependent type 11 collagen release from cartilage. Because levels of all these proinflammatory cytokines are raised in rheumatoid synovial fluids, this study suggests that IL17 may act as a potent upstream mediator of cartilage collagen breakdown in inflammatory joint diseases.

关键词：软骨/药物作用软骨/代谢胶原/药物作用胶原/代谢胶原Ⅱ型/药物作用胶原Ⅱ型/代谢复方合剂药物协同作用白细胞介素1/药理学白细胞介素17/药理学白细胞介素6/药理学金属内肽酶类/药理学抑瘤素M 肽类/药理学蛋白聚糖类动物牛

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Long term anti-tumour necrosis factor α monotherapy in rheumatoid arthritis:: effect on radiological course and prognostic value of markers of cartilage turnover and endothelial activation

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ANNALS OF THE RHEUMATIC DISEASES 2002年第4期61卷 311-318页

作者： den Broeder, AA Joosten, LAB Saxne, T Heinegård, D Fenner, H Miltenburg, AMM Frasa, WLH van Tits, LJ Buurman, WA van Riel, PLCM van de Putte, LBA Barrera, P Univ Med Ctr Nijmegen Dept Rheumatol NL-6500 HB Nijmegen Netherlands Univ Lund Hosp Dept Rheumatol S-22185 Lund Sweden Univ Lund Hosp Dept Cell & Mol Biol S-22185 Lund Sweden Organon Management Immunol Programme Oss Netherlands

Objectives: To investigate the effect of prolonged neutralisation of tumour necrosis factor alpha (TNFalpha) on the radiological course in rheumatoid arthritis (RA). To assess whether the radiological course can be predicted by clinical variables or biological markers of cartilage and synovium turnover and of endothelial activation. Patients and methods: Forty seven patients with active RA enrolled at our centre in monotheropy trials with adalimumab (D2E7), a fully human anti-TNFalpha monoclonal antibody, were studied for two years. Radiographs of hands and feet obtained at baseline and after one and two years were scored in chronological order by a single, blinded observer using the modified Sharp method. Radiological course was classified as stable or progressive using the smallest detectable difference as cut off point. The relation between radiological course and serum markers of cartilage and synovium turnover (metalloproteinases (MMP-1 and MMP-3), cartilage oligomeric matrix protein (COMP), human cartilage glycoprotein-39 (HC gp-39)), endothelial activation (soluble E-selectin and intercellular adhesion molecule (ICAM-1)), and integrated measures of disease activity were assessed using univariate and multivariate analysis. Results: Radiological evaluation was performed in 36 patients with paired sets of radiographs at baseline and two years. After two years a total of 15/36 (42%) presented no radiological progression. More patients with stable radiological course were still receiving anti-TNFa treatment after two years (13/15 (87%) Y 11/21 (52%);p=0.03) and had lower baseline COMP and sICAM-1 levels (p=0.01 and 0.04, respectively) than those in the group with progressive disease. In a logistic regression model the combination of sustained TNF neutralisation and baseline COMP and sICAM-1 levels was predictive for radiological outcome (p=0.03). C reactive protein and disease activity score area under the curve were significantly correlated with changes in radiol

关键词：抗体单克隆/治疗应用抗体单克隆人关节炎类风湿/诊断显像关节炎类风湿/治疗软骨/代谢细胞黏附分子/代谢随访研究 Logistic模型放射摄影术治疗结果肿瘤坏死因子α/拮抗剂和抑制剂肿瘤坏死因子α/免疫学女(雌)性人类男(雄)性中年人

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Diminished callus size and cartilage synthesis in α1β1 integrin-deficient mice during bone fracture healing

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AMERICAN JOURNAL OF PATHOLOGY 2002年第5期160卷 1779-1785页

作者： Ekholm, E Hankenson, KD Uusitalo, H Hiltunen, A Gardner, H Heino, J Penttinen, R Univ Turku Dept Med Biochem & Mol Biol FIN-20520 Turku Finland Univ Turku Dept Surg FIN-20520 Turku Finland Univ Turku MediCity Res Lab FIN-20520 Turku Finland Biogen Ltd Cambridge MA USA Univ Michigan Ortopaed Res Labs Ann Arbor MI 48109 USA

Integrins mediate cell adhesion to extracellular matrix components. Integrin alpha1/beta1 is a collagen receptor expressed on many mesenchymal cells, but mice deficient in alpha1 integrin (alpha1-KO) have no gross structural defects. Here, the regeneration of a fractured long bone was studied in alpha1-KO mice. These mice developed significantly less callus tissue than the wild-type (WT) mice, and safranin staining revealed a defect in cartilage formation. The mRNA levels of nine extracellular matrix genes in calluses were evaluated by Northern blotting. During the first 9 days the mRNA levels of cartilage-related genes, including type II collagen, type IX collagen, and type X collagen, were lower in alpha1-KO mice than in WT mice, consistent with the reduced synthesis of cartilaginous matrix appreciated in tissue sections. Histological observations also suggested a diminished number of chondrocytes in the alpha1-KO callus. Proliferating cell nuclear antigen staining revealed a reduction of mesenchymal progenitors at the callus site. Although, the number of mesenchymal stem cells (MSCs) obtained from WT and alpha1-KO whole marrow was equal, in cell culture the proliferation rate of the MSCs of alpha1-KO mice was slower, recapitulating the in vivo observation of reduced callus cell proliferation. The results demonstrate the importance of proper collagen-integrin interaction in fracture healing and suggest that alpha1 integrin plays an essential role in the regulation of MSC proliferation and cartilage production.

关键词：软骨蛋白聚糖类骨痂/代谢骨痂/病理生理学软骨/代谢软骨/病理生理学细胞分裂/生理学胶原/遗传学细胞外基质蛋白质类骨折愈合/生理学骨折/病理生理学基因型整合素α1β1 整合素类/缺乏整合素类/遗传学外源凝集素类 C型中胚层/细胞学小鼠近交系小鼠基因敲除蛋白聚糖类/遗传学 RNA 信使/遗传学 RNA 信使/代谢动物小鼠

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Application to a cartilage targeting strategy:: Synthesis and in vivo biodistribution of ¹⁴C-labeled quaternary ammonium-glucosamine conjugates

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BIOCONJUGATE CHEMISTRY 2000年第2期11卷 212-218页

作者： Giraud, I Rapp, M Maurizis, JC Madelmont, JC INSERM U484 F-63005 Clermont Ferrand France

As part of a cartilage targeting program based on the affinity of the quaternary ammonium (QA) moiety for cartilage, QA derivatives of D-glucosamine (DG), an antirheumatic drug exhibiting a natural tropism for cartilaginous tissues, were designed and evaluated by pharmacokinetic studies. Two QA-DG conjugates were synthesized and labeled with C-14 by cross-linking the QA entity (trimethylammonium or pyridinium) to [C-14]DG via an amide bond in a two-step procedure. After intravenous injection to male Sprague-Dawley rats, the two C-14-labeled conjugates exhibited similar pharmacokinetic profiles, but their behavior clearly differed from that of unconjugated DG in several ways. (i) The tissue distribution for the conjugates was more restricted, with a decreased radioactivity level for whole tissues except for kidney, cartilage, and skin. (ii) The radioactivity concentrated more rapidly and strongly in cartilage for the conjugates than for DG for the short times after injection;on the other hand, 1 h after administration, the radioactivity level in cartilage was higher for DG, this result being consistent with the tropism already observed for this compound. (iii) Both conjugates were eliminated predominantly by the urinary route (85%);the radioactivity level in urine for DG was lower (45% of the injected dose), and significant (CO2)-C-14 was found in expired air, indicating metabolization and utilization of DG for energy-consuming processes. (iv) Blood and plasma kinetics studies displayed an enterohepatic cycle for DG, whereas for the QA conjugates, a rapid disappearance was observed. (v) HPLC analyses of plasma and urine indicated a low degree of metabolization for the conjugates, most of the radioactivity recovered in urine and plasma corresponding to the unchanged molecule. This study demonstrates that the introduction of the QA moiety on DG modifies its biodistribution and lends it a greater specificity for cartilage, at least for short times after injection. These

关键词：抗风湿药/投药和剂量抗风湿药/化学抗风湿药/药代动力学生物利用度血液化学分析碳放射性同位素/血液碳放射性同位素/诊断应用碳放射性同位素/尿软骨/代谢色谱法高压液相药物载体/化学药物载体/药代动力学药物释放系统/方法粪便/化学葡糖胺/投药和剂量葡糖胺/化学葡糖胺/药代动力学分子结构季胺类化合物/化学大鼠 Sprague-Dawley 组织分布尿/化学动物男(雄)性大鼠

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Cartilage-specific matrix protein chondromodulin-I is associated with chondroid formation in salivary pleomorphic adenomas -: Immunohistochemical analysis

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AMERICAN JOURNAL OF PATHOLOGY 2001年第4期158卷 1465-1472页

作者： Kusafuka, K Hiraki, Y Shukunami, C Yamaguchi, A Kayano, T Takemura, T Japanese Red Cross Med Ctr Dept Pathol Shibuya Ku Tokyo 1508935 Japan Kyoto Univ Inst Frontier Med Sci Dept Mol Interact & Tissue Engn Kyoto Japan Nagasaki Univ Sch Dent Dept Oral Pathol Nagasaki 852 Japan Tokyo Med & Dent Univ Grad Sch Dept Int Hlth Dev Div Publ HlthSect Forens Dent Tokyo Japan

Chondromodulin-I (ChM-I) is a novel cartilage-specific matrix protein, in the growth plates of the long bones, ChM-I was shown to be expressed in mature to upper hypertrophic chondrocytes, and to be deposited in the cartilage matrix, As ChM-I strongly inhibits angiogenesis, cartilage is avascular, Also, ChM-I has bifunctional activity against chondrocyte proliferation, On the other hand, pleomorphic adenomas of the salivary glands frequently have chondroid elements. To elucidate the relationship between chondroid formation and hypovascularity in salivary pleomorphic adenomas, we immunohistochemically examined the expression and localization of ChM-I in 35 cases of this tumor. ChM-I was immunolocalized to the lacunae in the chondroid elements of pleomorphic adenomas (100%). Type II collagen and aggrecan were immunolocalized throughout the matrix around lacuna cells of the chondroid element (100%, 91.7%), and ChM-I was infrequently immunolocalized to the spindle-shaped myoepithelial cells in the myxoid element (37.5%). Fibroblast growth factor-2 was strongly immunolocalized to the lacuna cells in the chondroid element (100%), among the neoplastic myoepithelial cells in the myxoid elements (96.9%), and on the basement membranes around the solid nests of neoplastic myoepithelial cells (71.4%). Although CD34 is a marker of endothelial cells, CD34 was expressed in the endothelial cells in only a few areas around the epithelial elements and in the fibrous element of pleomorphic adenomas, No signals for CD34 were observed in chondroid elements in pleomorphic adenomas (P < 0.001), but a few signals were seen in the myxoid elements (P < 0.05), These findings suggested that lacuna cells and neoplastic myoepithelial cells expressed ChM-I, and that this molecule may play an important role in hypovascularity and chondroid differentiation in pleomorphic adenoma. In conclusion, pleomorphic adenoma expressed ChM-I, which is involved in hypovascularity and chondroid formation in this

关键词：腺瘤多形性/代谢腺瘤多形性/病理学软骨蛋白聚糖类抗原 CD34/代谢软骨/代谢软骨细胞/病理学胶原/代谢细胞外基质蛋白质类成纤维细胞生长因子2/代谢生长物质/代谢免疫组织化学胞间信号肽类和蛋白质类外源凝集素类 C型膜蛋白质类蛋白聚糖类/代谢涎腺肿瘤/代谢涎腺肿瘤/病理学人类

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