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Basic fibroblast growth factor inhibits osteoclast formation induced by 1α,25-dihydroxyvitamin D₃ through suppressing the production of osteoclast differentiation factor

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BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 1999年第1期265卷 45-50页

作者： Nakagawa, N Yasuda, H Yano, K Mochizuki, S Kobayashi, N Fujimoto, H Yamaguchi, K Shima, N Morinaga, T Higashio, K Snow Brand Milk Prod Co Ltd Res Inst Life Sci Ishibashi Tochigi 3290512 Japan

Basic fibroblast growth factor (bFGF) inhibited osteoclast-like cell (OCL) formation in cocultures of mouse spleen cells with either osteoblasts or a stromal cell line, ST2, in the presence of 1 alpha,25-dihydroxyvitamin D-3 [1,25(OH)(2)D-3]. bFGF directly acted on osteoblasts/stromal cells, but not osteoclast progenitors, to inhibit 1,25(OH)(2)D-3-induced OCL formation, bFGF suppressed the mRNA expression of osteoclast differentiation factor (ODF) but did not affect that of osteoclastogenesis inhibitory factor (OCIF) in ST2 cells treated with 1,25(OH)(2)D-3 and dexamethasone. Enzyme-linked immunosorbent assay showed that bFGF :hardly affected OCIF production in the treated ST2 cells. A genetically engineered soluble form of ODF, but not anti-OCIF neutralizing antibody, abolished bFGF-mediated inhibition of OCL formation, bFGF suppressed the binding of I-125-labeled OCIF to both ST2 cells and osteoblasts treated with 1,25(OH)(2)D-3. These findings indicate that bFGF inhibits 1,25(OH)(2)D-3-induced OCL formation via suppression of ODF production by osteoblasts/stromal cells. (C) 1999 Academic Press.

关键词：抗体/药理学骨化三醇/药理学载体蛋白质类/遗传学共同培养技术地塞米松/药理学成纤维细胞生长因子2/药理学糖蛋白类/遗传学糖蛋白类/药理学糖蛋白类/生理学动力学膜糖蛋白类/遗传学破骨细胞/细胞学破骨细胞/药物作用破骨细胞/生理学骨保护素 RANK配体 RNA 信使/遗传学核因子κB受体活化因子受体胞质和核受体肿瘤坏死因子重组蛋白质类/药理学脾/细胞学间质细胞/细胞学间质细胞/药物作用转录遗传动物人类小鼠

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Birth and death of bone cells: Basic regulatory mechanisms and implications for the pathogenesis and treatment of osteoporosis

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ENDOCRINE REVIEWS 2000年第2期21卷 115-137页

作者： Manolagas, SC Univ Arkansas Med Sci Sch Med Ctr Osteoporosis & Metab Bone Dis Div Endocrinol & Metab Little Rock AR 72205 USA Cent Arkansas Vet Healthcare Syst Little Rock AR 72205 USA

The adult skeleton regenerates by temporary cellular structures that comprise teams of juxtaposed osteoclasts and osteoblasts and replace periodically old bone with new. A considerable body of evidence accumulated during the last decade has shown that the rate of genesis of these two highly specialized cell types, as well as the prevalence of their apoptosis, is essential for the maintenance of bone homeostasis;and that common metabolic bone disorders such as osteoporosis result largely from a derangement in the birth or death of these cells. The purpose of this article is 3-fold: 1) to review the role and the molecular mechanism of action of regulatory molecules, such as cytokines and hormones, in osteoclast and osteoblast birth and apoptosis;2) to review the evidence for the contribution of changes in bone cell birth or death to the pathogenesis of the most common forms of osteoporosis;and 3) to highlight the implications of bone cell birth and death for a better understanding of the mechanism of action and efficacy of present and future pharmacotherapeutic agents for osteoporosis.

关键词：细胞凋亡骨和骨组织/病理学细胞因子类/生理学激素类/生理学成骨细胞/病理学成骨细胞/生理学破骨细胞/病理学破骨细胞/生理学骨生成骨质疏松/病因学骨质疏松/治疗动物人类

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Equine osteoclast-like cells generated in vitro demonstrate similar characteristics to directly isolated mature osteoclasts

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RESEARCH IN VETERINARY SCIENCE 2000年第2期68卷 161-167页

作者： Gray, AW Davies, ME Jeffcott, LB Univ Cambridge Dept Clin Vet Med Equine Orthopaed Res Grp Cambridge CB3 0ES England

We report on novel methods to isolate osteoclasts (ocs) and generate osteoclast-like cells (OCLS) from the bone and bone marrow of the equine femur, OCS were successfully isolated from bone scrapings taken from the endosteal surface of the femurs of three horses. OCLs Were generated from bone marrow cells taken from the same animals. The validity of using the formation of OCLS as a method for studying OC differentiation and activity was confirmed by the similar characteristics of these two cells. In particular, they both were multinuclear, expressed the enzyme tartrate resistant acid phosphatase and the vitronectin receptor. Most importantly, both were able to resorb bone as demonstrated by the formation of extensive resorption pits when cultured on dentine slices. The generation of OCLS from bone marrow obtained from the equine femur can therefore be used to study equine cc differentiation and for studies requiring the generation of large numbers of these cells. ocs isolated directly from the same bones may be used to examine the effect of a variety of factors on bone resorption in vitro and to continually reaffirm the validity of using OCLS for large-scale studies on OC biology. Such research is essential for improved understanding of bone turnover and endochondral ossification in the horse. (C) 2000 Harcourt Publishers Ltd.

关键词：骨质吸收细胞培养的马/生理学免疫组织化学破骨细胞/生理学受体玻连蛋白/分析动物

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A new member of tumor necrosis factor ligand family, ODF/OPGL/TRANCE/RANKL, regulates osteoclast differentiation and function

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BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 1999年第3期256卷 449-455页

作者： Takahashi, N Udagawa, N Suda, T Showa Univ Sch Dent Dept Biochem Shinagawa Ku Tokyo 1428555 Japan

Osteoclasts, the multinucleated giant cells that resorb bone, develop from monocyte-macrophage lineage cells. Osteoblasts or bone marrow stromal cells have been suggested to be involved in osteoclastic bone resorption, The recent discovery of new members of the tumor necrosis factor (TNF) receptor-ligand family has elucidated the precise mechanism by which osteoblasts/stromal cells regulate osteoclast differentiation and function. Osteoblasts/stromal cells express a new member of the TNF-Ligand family "osteoclast differentiation factor(ODF)/osteoprotegerin ligand (OPGL)/TNF-related activation-induced cytokine (TRANCE)/receptor activator of NF-kB ligand (RANKL)" as a membrane associated factor. Osteoclast precursors which possess RANK, a TNF receptor family member, recognize ODF/OPGL/TRANCE/RANKL through cell-to-cell interaction with osteoblasts/stromal cells, and differentiate into osteoclasts in the presence of macrophage colony-stimulating factor. Mature osteo clasts also express RANK, and their bone-resorbing activity is also induced by ODF/OPGL/TRANCE/RANKL which osteoblasts/stromal cells possess. Osteoprotegerin (OPG)/osteoclastogenesis inhibitory factor (OCIF)/TNF receptor-like molecule 1 (TR1) is a soluble decoy receptor for ODF/OPGL/TRANCE/RANKL, Activation of NF-kB and c-Jun N-terminal kinase through the RANK-mediated signaling system appears to be involved in differentiation and activation of osteoclasts, (C) 1999 Academic Press.

关键词：载体蛋白质类细胞分化配体膜糖蛋白类/化学膜糖蛋白类/遗传学膜糖蛋白类/生理学成骨细胞/生理学破骨细胞/细胞学破骨细胞/生理学 RANK配体核因子κB受体活化因子受体肿瘤坏死因子/化学受体肿瘤坏死因子/生理学信号传导肿瘤坏死因子α/化学肿瘤坏死因子α/生理学动物小鼠

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A common downstream signaling activity of osteoclast survival factors that prevent nitric oxide-promoted osteoclast apoptosis

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ENDOCRINOLOGY 2000年第8期141卷 2995-3005页

作者： Kanaoka, K Kobayashi, Y Hashimoto, F Nakashima, T Shibata, M Kobayashi, K Kato, Y Sakai, H Nagasaki Univ Sch Dent Dept Pharmacol Nagasaki 8528588 Japan Nagasaki Univ Sch Dent Dept Orthodont Nagasaki 8528588 Japan

Treatment with NO-releaser NOC18 significantly promoted apoptosis in murine osteoclast-like cells, with a transient increase in caspase-3-like protease activity. In contrast, the apoptosis was protected against by caspase inhibitors, most efficiently with the broadly acting caspase specific inhibitor z-Asp-CH2-DCB, indicating involvement of multiple caspases in progression of the apoptosis. Among osteoclast survival factors examined, calcitonin completely protected against morphologically defined-apoptosis and the increase of caspase-3-like protease activity. The effect of calcitonin was mimicked by treatment of cells with (Bu)(2)cAMP and forskolin, and abolished by protein kinase-A inhibitor H-89. Independently from the PKA activation, colony stimulating factor-1, interleukin-1 beta and the receptor activator of NF-kappa B ligand also protected against the apoptosis but were less effective than calcitonin. All survival factors investigated inhibited conversion of procaspases-3 and -9 to their mature forms in the cells. Thus, downstream antiapoptotic signaling activity from each factor overlapped in inhibition of caspases. However, how this was attained seemed to be different from each other. Typically, only colony stimulating factor-1 up-regulated expression of endogenous caspase inhibitor protein, X-linked inhibitor of apoptosis (XIAP), in the osteoclast-like cells.

关键词：细胞凋亡/药物作用布拉地新/药理学降钙素/药理学半胱氨酸天冬氨酸蛋白酶/代谢细胞存活/药物作用细胞培养的共同培养技术环AMP依赖性蛋白激酶类/拮抗剂和抑制剂酶抑制剂/药理学福司柯林/药理学白细胞介素1/药理学异喹啉类/药理学一氧化氮/药理学一氧化氮供体/药理学亚硝基化合物/药理学破骨细胞/生理学信号传导磺胺类动物男(雄)性小鼠兔

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Modulation of osteoclast differentiation and function by the new members of the tumor necrosis factor receptor and ligand families

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ENDOCRINE REVIEWS 1999年第3期20卷 345-357页

作者： Suda, T Takahashi, N Udagawa, N Jimi, E Gillespie, MT Martin, TJ Showa Univ Sch Dent Dept Biochem Shinagawa Ku Tokyo 1428555 Japan Univ Melbourne St Vincents Inst Med Res Fitzroy Vic 3065 Australia

I. Introduction

关键词：载体蛋白质类/生理学细胞分化配体膜糖蛋白类/生理学成骨细胞/生理学破骨细胞/细胞学破骨细胞/生理学 RANK配体核因子κB受体活化因子受体肿瘤坏死因子/生理学间质细胞/生理学动物人类

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Basic fibroblast growth factor induces osteoclast formation by reciprocally regulating the production of osteoclast differentiation factor and osteoclastogenesis inhibitory factor in mouse osteoblastic cells

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BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 1999年第1期265卷 158-163页

作者： Nakagawa, N Yasuda, H Yano, K Mochizuki, S Kobayashi, N Fujimoto, H Shima, N Morinaga, T Chikazu, D Kawaguchi, H Higashio, K Snow Brand Milk Prod Co Ltd Life Sci Res Inst Ishibashi Tochigi 3290512 Japan Univ Tokyo Fac Med Dept Orthopaed Surg Tokyo 1138655 Japan

Basic fibroblast growth factor (bFGF) induced osteoclast formation in co-cultures of mouse spleen cells and osteoblasts. Osteoclastogenesis inhibitory factor (OCIF) and a selective cylooxygenase-2 (COX-2) inhibitor, NS-398, abolished bFGF-induced osteoclast formation. bFGF did not affect spleen cells, but it did affect osteoblasts, to stimulate osteoclast formation. Northern blot analysis revealed that bFGF up-regulated the expression of osteoclast differentiation factor (ODF) and COX-2 and down-regulated the expression of OCIF in primary osteoblastic cells. NS-398 abolished the increase of ODF mRNA, but it had no effect on the decrease of OCIF mRNA NS-398 suppressed the binding of I-125-labeled OCIF to osteoblastic cells treated with bFGF, Enzyme-linked immunosorbent assay showed that bFGF inhibited OCIF production by osteoblastic cells, and the inhibition was not affected by NS-398. We conclude that bFGF induces osteoclast formation by stimulating ODF production through COX-2-mediated prostaglandin synthesis and by suppressing OCIF production through a mechanism independent of prostaglandin synthesis. (C) 1999 Academic Press.

关键词：动物新生载体蛋白质类/遗传学载体蛋白质类/药理学载体蛋白质类/生理学共同培养技术环氧化酶2 环氧化酶2抑制剂环加氧酶抑制药/药理学成纤维细胞生长因子2/药物作用成纤维细胞生长因子2/药理学基因表达调控/药物作用基因表达调控/生理学糖蛋白类/遗传学糖蛋白类/生理学同工酶类/代谢膜糖蛋白类/遗传学膜糖蛋白类/药理学膜糖蛋白类/生理学膜蛋白质类小鼠近交系硝基苯甲酸盐/药理学破骨细胞/细胞学破骨细胞/药物作用破骨细胞/生理学骨保护素前列腺素内过氧化物合酶类/代谢 RANK配体核因子κB受体活化因子受体胞质和核受体肿瘤坏死因子重组蛋白质类/药理学脾/细胞学磺胺类/药理学转录遗传/药物作用动物人类小鼠

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Parathyroid hormone temporal effects on bone formation and resorption

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BULLETIN OF MATHEMATICAL BIOLOGY 2000年第1期62卷 163-188页

作者： Kroll, MH Johns Hopkins Med Inst Dept Pathol Baltimore MD 21287 USA

Parathyroid hormone (PTH) paradoxically causes net bone loss (resorption) when administered in a continuous fashion, and net bone formation (deposition) when administered intermittently. Currently no pharmacological formulations are available to promote bone formation, as needed for the treatment of osteoporosis. The paradoxical behavior of PTH confuses endocrinologists, thus, a model bone resorption or deposition dependent on the timing of PTH administration would de-mystify this behavior and provide the basis for logical drug formulation. We developed a mathematical model that accounts for net bone loss with continuous PTH administration and net bone formation with intermittent PTH administration, based on the differential effects of PTH on the osteoblastic and osteoclastic populations of cells. Bone, being a major reservoir of body calcium, is under the hormonal control of PTH. The overall effect of PTH is to raise plasma levels of calcium, partly through bone resorption. Osteoclasts resorb bone and liberate calcium, but they lack receptors for PTH. The preosteoblastic precursors and preosteoblasts possess receptors for PTH, upon which the hormone induces differentiation from the precursor to preosteoblast and from the preosteoblast to the osteoblast. The osteoblasts generate IL-6;IL-6 stimulates preosteoclasts to differentiate into osteoclasts. We developed a mathematical model for the differentiation of osteoblastic and osteoclastic populations in bone, using a delay time of 1 hour for differentiation of preosteoblastic precursors into preosteoblasts and 2 hours for the differentiation of preosteoblasts into osteoblasts. The ratio of the number of osteoblasts to osteoclasts indicates the net effect of PTH on bone resorption and deposition;the timing of events producing the maximum ratio would induce net bone deposition. When PTH is pulsed with a frequency of every hour, the preosteoblastic population rises and decreases in nearly a symmetric pattern, with 3.9 p

关键词：骨重建/药物作用骨重建/生理学计算机模拟模型生物学成骨细胞/药物作用成骨细胞/生理学破骨细胞/药物作用破骨细胞/生理学骨质疏松/药物疗法骨质疏松/预防和控制甲状旁腺素/投药和剂量甲状旁腺素/药理学甲状旁腺素/生理学时间因素老年人动物女(雌)性人类大鼠

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Activation of osteoclasts by interleukin-1: Divergent responsiveness in osteoclasts formed in vivo and in vitro

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JOURNAL OF CELLULAR PHYSIOLOGY 2000年第3期184卷 334-340页

作者： Fox, SW Fuller, K Chambers, TJ St George Hosp Sch Med Dept Histopathol London SW17 0RE England

Recently, it has been found that osteoclasts are induced and activated by osteoblastic cells through expression of receptor activator NF-kB ligand (RANKL), and that soluble recombinant RANKL, with M-CSF, can replace the need for osteoblastic cells in osteoclast formation. We exploited this opportunity to compare the responsiveness of osteoclast-like cells (OCL) formed in vitro in the absence of osteoblasts, with that of osteoclasts ex vivo. We found that while OCL responded to several hormones and cytokines like ex vivo osteoclasts, their responsiveness to interleukin-1 (IL-1) was fundamentally different: IL1 directly stimulated actin ring formation in OCL, but had no effect on actin rings or survival in osteoclasts ex vivo unless osteoblastic cells were present. This difference could not be attributed to the use of plastic culture substrates for OCL formation, nor to osteoblastic contamination, and did not seem to be mediated by the macrophages that form in OCL cultures. To understand the mechanisms by which IL-1 induces bone loss, it will need to be determined whether or not IL-1-responsive OCLs have a counterpart in vivo. Whichever is the case, our data suggest that the behavior of osteoclasts formed in culture will not always predict that of osteoclasts in vivo. J. Cell. Physiol. 184:334-340, 2000. (C) 2000 Wiley-Liss, Inc.

关键词：肌动蛋白类/代谢骨质吸收/病因学骨质吸收/病理学载体蛋白质类/药理学细胞分化/药物作用细胞存活/药物作用细胞培养的白细胞介素1/药理学巨噬细胞集落刺激因子/药理学膜糖蛋白类/药理学破骨细胞/细胞学破骨细胞/药物作用破骨细胞/生理学 RANK配体核因子κB受体活化因子动物小鼠

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Leptin inhibits bone formation through a hypothalamic relay: A central control of bone mass

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CELL 2000年第2期100卷 197-207页

作者： Ducy, P Amling, M Takeda, S Priemel, M Schilling, AF Beil, FT Shen, JH Vinson, C Rueger, JM Karsenty, G Baylor Coll Med Dept Mol & Human Genet Houston TX 77030 USA Univ Hamburg Dept Trauma Surg D-20246 Hamburg Germany NCI Biochem Lab Bethesda MD 20892 USA

Gonadal failure induces bone loss while obesity prevents it. This raises the possibility that bone mass, body weight, and gonadal function are regulated by common pathways. To test this hypothesis, we studied leptin-deficient and leptin receptor-deficient mice that are obese and hypogonadic. Both mutant mice have an increased bone formation leading to high bone mass despite hypogonadism and hypercortisolism. This phenotype is dominant, independent of the presence of fat, and specific for the absence of leptin signaling. There is no leptin signaling in osteoblasts but intracerebroventricular infusion of leptin causes bone loss in leptin-deficient and wild-type mice. This study identifies leptin as a potent inhibitor of bone formation acting through the central nervous system and therefore describes the central nature of bone mass control and its disorders.

关键词：骨密度/遗传学骨重建/药物作用骨重建/遗传学载体蛋白质类/遗传学载体蛋白质类/代谢细胞培养的下丘脑/生理学注射脑室内瘦素/遗传学瘦素/代谢瘦素/药理学小鼠近交C57BL 小鼠肥胖小鼠转基因神经肽Y/生理学肥胖症/遗传学肥胖症/代谢成骨细胞/生理学破骨细胞/细胞学破骨细胞/生理学骨质疏松/遗传学骨质疏松/代谢表型受体细胞表面信号传导/生理学动物小鼠

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