Osteoblast/osteocyte-specific inactivation of Stat3 decreases load-driven bone formation and accumulates reactive oxygen species
Osteoblast/osteocyte-specific inactivation of Stat3 decreases load-driven bone formation and accumulates reactive oxygen species
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DOI：
10.1016/j.bone.2011.04.020
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发表时间：
2011-09-01
期刊：
影响因子：
4.1
通讯作者：
Li, Jiliang
中科院分区：
文献类型：
--
作者：
Zhou, Hongkang;Newnum, America B.;Li, Jiliang
转录信号转导子和激活子 3 (Stat3) 是一种在多种细胞类型中表达的转录因子，包括成骨细胞、骨细胞和破骨细胞。 STAT3 突变会导致一种罕见的人类免疫缺陷疾病，表现为骨矿物质密度降低和复发性病理性骨折。为了研究 Stat3 在负荷驱动的骨代谢中的作用，产生了两种成骨细胞/骨细胞选择性 Stat3 敲除 (KO) 小鼠品系。与年龄匹配的同窝对照相比，Stat3 的选择性失活显着降低了骨矿物质密度（7-12%，p
Signal transducers and activators of transcription 3 (Stat3) is a transcription factor expressed in many cell types including osteoblasts, osteocytes, and osteoclasts. STAT3 mutations cause a rare human immunodeficiency disease that presents reduced bone mineral density and recurrent pathological fractures. To investigate the role of Stat3 in load-driven bone metabolism, two strains of osteoblast/osteocyte-selective Stat3 knockout (KO) mice were generated. Compared to age-matched littermate controls, this selective inactivation of Stat3 significantly lowered bone mineral density (7-12%, p