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首页> 外文期刊>Journal of Cellular Physiology >Dok-1 and Dok-2 deficiency induces osteopenia via activation of osteoclasts.
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Dok-1 and Dok-2 deficiency induces osteopenia via activation of osteoclasts.

机译：Dok-1和Dok-2不足导致骨量减少通过激活破骨细胞。

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Osteoporosis causes fractures that lead to reduction in the quality of life and it is one of the most prevalent diseases as it affects approximately 10% of the population. One of the important features of osteoporosis is osteopenia. However, its etiology is not fully elucidated. Dok-1 and Dok-2 are adaptor proteins acting downstream of protein tyrosine kinases that are mainly expressed in the cells of hematopoietic lineage. Although these proteins negatively regulate immune system, their roles in bone metabolism are not understood. Here, we analyzed the effects of Dok-1 and Dok-2 double-deficiency on bone. Dok-1/2 deficiency reduced the levels of trabecular and cortical bone mass compared to wildtype. In addition, Dok-1/2 deficiency increased periosteal perimeters and endosteal perimeters of the mid shaft of long bones. Histomorphometric analysis of the bone parameters indicated that Dok-1/2 deficiency did not significantly alter the levels of bone formation parameters including mineralizing surface/bone surface (MS/BS), mineral apposition rate (MAR) and bone formation rate (BFR). In contrast, Dok-1/2 deficiency enhanced the levels of bone resorption parameters including osteoclast number (N.Oc/BS) and osteoclast surface (Oc.S/BS). Analyses of individual osteoclastic activity indicated that Dok-1/2 deficiency enhanced pit formation. Systemically, Dok-1/2 deficiency increased the levels of urinary deoxypyridinoline (Dpyr). Search for the target point of the Dok-1/2 deficiency effects on osteoclasts identified that the mutation enhanced sensitivity of osteoclast precursors to macrophage colony-stimulating factor. These data revealed that Dok-1 and Dok-2 deficiency induces osteopenia by activation of osteoclasts.
机译：骨质疏松症导致骨折导致生活质量和减少之一最普遍的疾病,因为它影响大约10%的人口。骨质疏松症的重要特征是骨量减少。然而,它的病因尚未完全阐明。Dok-1和Dok-2适配器蛋白质作用下游的蛋白酪氨酸激酶主要表达于造血细胞血统。调节免疫系统,他们的角色在骨头新陈代谢不理解。Dok-1的影响和Dok-2 double-deficiency在骨头。骨小梁和皮质骨量相比野生型。骨膜周长增加,骨内膜的周边的轴长骨头。Histomorphometric骨骼的分析参数表明Dok-1/2缺没有大大改变骨形成的水平参数包括矿化表面/骨表面(女士/ BS)、矿物附着率(3月)和骨形成率(BFR)。缺Dok-1/2增强骨的水平吸收参数包括破骨细胞数量(N.Oc / BS)和破骨细胞表面(Oc.S / BS)。分析个人的监测活动表明Dok-1/2缺乏加强坑形成。增加尿deoxypyridinoline的水平(Dpyr)。Dok-1/2缺乏对破骨细胞的影响确定突变增强敏感性巨噬细胞的破骨细胞前体集落刺激因子。Dok-1 Dok-2不足引起骨量减少破骨细胞的激活。

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