没有脑5 -羟色胺的成年Tph2基因敲除小鼠脊柱小梁骨中度升高,但皮质骨厚度中度降低。

BoneKEy reports Pub Date : 2015-07-15 eCollection Date: 2015-01-01 DOI:10.1038/bonekey.2015.87
Robert Brommage, Jeff Liu, Deon Doree, Wangsheng Yu, David R Powell, Qi Melissa Yang
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引用次数: 17

摘要

通过敲除小鼠色氨酸羟化酶(外周Tph1和神经元Tph2)基因来破坏神经元和外周血清素合成,据称可以降低(Tph2 KO)和增加(Tph1 KO)骨量。在本报告中,观察到成年雄性和雌性Tph2 KO小鼠脊柱小梁骨升高。雌性Tph2 KO小鼠股骨中轴皮质骨厚度减少。作为Tph1/Tph2双敲除(DKO)小鼠队列的一部分,雄性和雌性Tph1 KO小鼠骨量正常。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Adult Tph2 knockout mice without brain serotonin have moderately elevated spine trabecular bone but moderately low cortical bone thickness.

Disruption of serotonin synthesis in neurons and the periphery by knockout (KO) of mouse genes for tryptophan hydroxylases (peripheral Tph1 and neuronal Tph2) has been claimed to decrease (Tph2 KO) and increase (Tph1 KO) bone mass. In this report, adult male and female Tph2 KO mice were observed to have elevated spine trabecular bone. Female Tph2 KO mice have reduced midshaft femur cortical bone thickness. Bone mass was normal in male and female Tph1 KO mice examined as part of a Tph1/Tph2 double knockout (DKO) mouse cohort.

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