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Angiotensin II suppresses osteoblastic differentiation and mineralized nodule formation via AT1 receptor in ROS17/2.8 cells

机译:血管紧张素II通过ROS17 / 2.8细胞中的AT1受体抑制成骨细胞分化和矿化结节形成

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摘要

IntroductionAngiotensin II (Ang II) not only regulates systemic blood pressure through a vasoconstrictive effect, but also promotes bone resorption. We recently reported that Ang II (10–6 M) stimulated the production of matrix metalloproteinases via the AT1 receptor in osteoblastic ROS17/2.8 cells, but suppressed alkaline phosphatase activity. However, the roles of Ang II in osteoblastic differentiation and the function of osteogenesis in osteoblasts are unclear. Therefore, we examined the effect of Ang II on the expression of osteogenesis-related transcription factors and extracellular matrix (ECM) proteins, as well as mineralized nodule formation in ROS17/2.8 cells.
机译:简介血管紧张素II(Ang II)不仅通过血管收缩作用调节全身血压,而且还促进骨吸收。我们最近报道,Ang II(10 –6 M)通过成骨细胞ROS17 / 2.8细胞中的AT1受体刺激了基质金属蛋白酶的产生,但抑制了碱性磷酸酶的活性。但是,Ang II在成骨细胞分化中的作用以及成骨细胞中成骨的功能尚不清楚。因此,我们研究了Ang II对成骨相关转录因子和细胞外基质(ECM)蛋白表达以及ROS17 / 2.8细胞中矿化结节形成的影响。

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