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首页> 外文期刊>Journal of Cellular Physiology >GATA-1 Deficiency Rescues Trabecular but not Cortical Bone in OPG Deficient Mice
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GATA-1 Deficiency Rescues Trabecular but not Cortical Bone in OPG Deficient Mice

机译：GATA-1缺乏救援小梁但不是皮质骨的功能有缺陷的老鼠

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GATA-1(low/low) mice have an increase in megakaryocytes (MKs) and trabecular bone. The latter is thought to result from MKs directly stimulating osteoblastic bone formation while simultaneously inhibiting osteoclastogenesis. Osteoprotegerin (OPG) is known to inhibit osteoclastogenesis and OPG(-/-) mice have reduced trabecular and cortical bone due to increased osteoclastogenesis. Interestingly, GATA-1(low/low) mice have increased OPG levels. Here, we sought to determine whether GATA-1 knockdown in OPG(-/-) mice could rescue the observed osteoporotic bone phenotype. GATA-1(low/low) mice were bred with OPG(-/-) mice and bone phenotype assessed. GATA-1(low/low) x OPG(-/-) mice have increased cortical bone porosity, similar toOPG(-/-) mice. Both OPG(-/-) and GATA-1(low/low) x OPG(-/-) mice, were found to have increased osteoclasts localized to cortical bone, possibly producing the observed elevated porosity. Biomechanical assessment indicates that OPG(-/-) and GATA-1(low/low) x OPG(-/-) femurs are weaker and less stiff than C57BL/6 or GATA-1(low/low) femurs. Notably, GATA-1(low/low) x OPG(-/-) mice had trabecular bone parameters that were not different from C57BL/6 values, suggesting that GATA-1 deficiency can partially rescue the trabecular bone loss observed with OPG deficiency. The fact that GATA-1 deficiency appears to be able to partially rescue the trabecular, but not the cortical bone phenotype suggests that MKs can locally enhance trabecular bone volume, but that MK secreted factors cannot access cortical bone sufficiently to inhibit osteoclastogenesis or that OPG itself is required to inhibit osteoclastogenesis in cortical bone. (C) 2014 Wiley Periodicals, Inc.
机译：GATA-1(低/低)小鼠的增加巨核细胞(MKs)和骨小梁。后者被认为直接从MKs结果刺激成骨细胞的骨形成同时抑制osteoclastogenesis。Osteoprotegerin(功能)是已知的抑制osteoclastogenesis和功能(- / -)小鼠减少了由于增加了骨小梁和皮质骨osteoclastogenesis。GATA-1(低/低)老鼠增加了功能水平。在这里,我们试图确定是否GATA-1可拆卸的功能(- / -)小鼠可以拯救观察骨质疏松性骨表型。GATA-1(低/低)老鼠繁殖功能(- / -)小鼠和骨表型评估。功能(- / -)小鼠增加皮质骨孔隙度,类似toOPG(- / -)小鼠。功能和GATA-1(低/低)x(- / -)小鼠,被发现增加了破骨细胞本地化皮质骨,可能生产高孔隙度。功能说明(- / -)和GATA-1 x(低/低)功能(- / -)股骨弱,那么僵硬C57BL / 6 GATA-1黄金(low low)股骨。GATA-1功能(低/低)x(- / -)小鼠小梁骨参数没有不同C57BL / 6的值,这表明GATA-1缺乏症可以部分救援小梁骨损失呢观察到的功能缺陷。GATA-1缺似乎能够部分小梁的救援,但不是皮质骨表现型表明MKs可以局部增强骨小梁体积,但这可分泌因素不能访问皮质骨充分抑制osteoclastogenesis或者功能本身需要抑制osteoclastogenesis皮质骨。

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