Regulation of skeletal mass, strength, and turnover by inhibin A.

机译：抑制素A对骨骼质量，强度和周转的调节。

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The goal of the studies in this dissertation was to directly test whether Inhibin A (InhA) regulates bone mass in vivo, using a transgenic model of inducible InhA overexpression. The data presented herein repeatedly demonstrate that InhA is a skeletal anabolic agent, in both the axial and appendicular skeleton, that acts through stimulation of osteoblast activity and differentiation. Interestingly, our current studies show that Inhibin is not only capable of stimulating bone formation in healthy intact mice, but is also effective in a number of pathological situations including prevention of gonadectomy-induced bone loss, acceleration of repair/regeneration in a model of extended bone formation (distraction osteogenesis, DO), and attenuation of disuse osteopenia (during hindlimb suspension, HS). In contrast, InhA was ineffective in its ability to affect the skeleton when overexpression was begun 4 weeks after orchidectomy in adult mice. This finding suggests that the behavior of osteoblasts or an indirect mediator of Inhibin action undergoes an unknown pathophysiological alteration in the face of untreated hypogonadism that reduces or eliminates the ability of the osteoblast to respond to Inhibin signaling.; The in vivo data in intact mice, during the prevention of gonadectomy-induced bone loss, and during DO all suggest that Inhibin stimulates the bone forming activity of mature osteoblasts. In addition, the results of the ex vivo osteoblast cultures from the Intact and Time Course Studies, the proliferating cell nuclear antigen staining of mice exposed to InhA during DO, and the HS study all suggest that InhA stimulates osteoblast recruitment, differentiation, and proliferation, processes that are intimately and inseparably linked. However, none of the assays in any of these studies found that InhA had a significant effect on osteoclastogenesis or bone resorption. Taken together these data lead us to conclude that the anabolic effects of in vivo InhA overexpression on the skeleton are mediated by stimulation of cells in the osteoblastic lineage.; The anabolic effects of Inhibin described here indicate that the Inhibin signaling pathway in the skeleton, once elucidated, may provide new targets for treating bone loss in a variety of conditions. Taken together, we hope that this information aids in understanding, preventing, and treating diseases of bone loss and fragility. (Abstract shortened by UMI.)

机译：本研究的目的是使用诱导型InhA过表达的转基因模型直接测试抑制素A（InhA）是否在体内调节骨量。本文提供的数据反复证明，InhA是在轴向和阑尾骨骼中的骨骼合成代谢药物，通过刺激成骨细胞活性和分化发挥作用。有趣的是，我们目前的研究表明，抑制素不仅能够刺激健康的完整小鼠的骨形成，而且在多种病理情况下也有效，包括预防性腺切除术引起的骨丢失，在扩展模型中加速修复/再生。骨形成（分散成骨，DO）和减少废骨减少（后肢悬吊，HS）。相反，成年小鼠兰花切除术后4周开始过度表达时，InhA对骨骼的影响无效。这一发现表明，成骨细胞或抑制素作用的间接介质的行为在未经治疗的性腺功能减退症面前经历了未知的病理生理改变，从而降低或消除了成骨细胞对抑制素信号传导的反应能力。在预防性腺切除术诱导的骨丢失期间以及在溶解氧期间，完整小鼠的体内数据均表明抑制素可刺激成熟成骨细胞的骨形成活性。此外，完整和时程研究的离体成骨细胞培养结果，DO期间暴露于InhA的小鼠的增殖细胞核抗原染色以及HS研究均表明InhA刺激成骨细胞的募集，分化和增殖，紧密联系在一起的过程。但是，这些研究均未发现InhA对破骨细胞生成或骨吸收有显着影响。综合这些数据，我们得出结论，体内InhA过表达对骨骼的合成代谢作用是由成骨细胞谱系中细胞的刺激介导的。此处描述的抑制素的合成代谢作用表明，一旦阐明，骨架中的抑制素信号传导途径可能会为在各种情况下治疗骨丢失提供新的靶点。综上所述，我们希望这些信息有助于理解，预防和治疗骨质流失和脆弱性疾病。（摘要由UMI缩短。）

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作者
Perrien, Daniel Scott.;
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作者单位

University of Arkansas for Medical Sciences.;

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授予单位 University of Arkansas for Medical Sciences.;
学科 Biology Cell.; Biology Animal Physiology.
学位 Ph.D.
年度 2006
页码 204 p.
总页数 204
原文格式 PDF
正文语种 eng
中图分类细胞生物学;生理学;
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Regulation of skeletal mass, strength, and turnover by inhibin A.

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