Genetic Disruption of All NO Synthase Isoforms Enhances BMD and Bone Turnover in Mice In Vivo: Involvement of the Renin‐Angiotensin System
Genetic Disruption of All NO Synthase Isoforms Enhances BMD and Bone Turnover in Mice In Vivo: Involvement of the Renin‐Angiotensin System
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DOI：
10.1359/jbmr.080107
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发表时间：
2008-05
影响因子：
6.2
通讯作者：
K. Sabanai;M. Tsutsui;A. Sakai;H. Hirasawa;Shinya Tanaka;Eiichiro Nakamura;A. Tanimoto;Y. Sasaguri-Y.-Sa
中科院分区：
文献类型：
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作者：
K. Sabanai;M. Tsutsui;A. Sakai;H. Hirasawa;Shinya Tanaka;Eiichiro Nakamura;A. Tanimoto;Y. Sasaguri-Y.-Sa
前言：NO由神经型(NNOS)、诱导型(INOS)和内皮型(ENOS)三种不同的一氧化氮合酶(NOS)亚型合成。NO在骨代谢中的作用已经在药理学研究和一氧化氮合酶异构体缺陷小鼠的研究中得到了广泛的研究。然而，由于药物的非特异性和一氧化氮合酶亚型之间的代偿性，内源性NO的最终作用仍然知之甚少。为了解决这一问题，我们成功地培育出了三种一氧化氮合酶基因都被完全破坏的小鼠。在这项研究中，我们检查了这些小鼠的骨代谢是否异常。
Introduction: NO is synthesized by three different NO synthase (NOS) isoforms, including neuronal (nNOS), inducible (iNOS) and endothelial NOS (eNOS). The roles of NO in bone metabolism have been extensively investigated in pharmacological studies and in studies with NOS isoform–deficient mice. However, because of the nonspecificity of agents and compensation among the NOS isoforms, the ultimate roles of endogenous NO are still poorly understood. To address this point, we successfully generated mice in which all three NOS genes are completely disrupted. In this study, we examined whether bone metabolism is abnormal in those mice.