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Lrp5通过抑制十二指肠中血清的合成来控制骨的形成

Vijay K Yadav¹, Je-Hwang Ryu, Nina Suda

¹Department of Genetics and Development, Columbia University, New York, NY 10032, USA.

|December 2, 2008

概括

较低的LRp5水平通过减少肠道血清素 (一种抑制骨形成的激素) 来增加骨质. 这项研究揭示了一个新的肠-骨轴,为骨损失提供了潜在的治疗方法.

科学领域:

骨生物学骨生物学
内分泌学在内分泌学.
遗传学遗传学是一个

背景情况:

Lrp5基因中的功能损失和功能增益突变影响骨形成,导致骨质疏松症或高骨质量.
Lrp5被认定为Wnt核心受体,但骨质细胞特异性β-catenin破坏不会影响骨形成.

研究的目的:

调查LRp5在调节骨形成中的作用,超出其已知的作为Wnt核心受体的功能.
确定LRp5影响骨质的机制,特别是与血清素生产有关的机制.

主要方法:

研究Lrp5对十二指肠Tph1基因表达的影响.
使用了具有特定Lrp5或Tph1变异的转基因小鼠 (肠特异性与骨质细胞特异性).
在各种实验小组中评估了骨质形成,骨质量和血清素水平.

主要成果:

发现lrp5抑制了Tph1的表达,Tph1是负责十二指肠中血清素合成的酶.
在Lrp5缺乏的小鼠中,降低的血清素水平使骨形成和骨质量正常化.
肠特异性Lrp5无活化减少了独立于β-catenin的骨形成.
肠特异性Lrp5激活或Tph1非激活增加了骨质量,并防止了卵巢切除诱导的骨质损失.
血清素通过Htr1b受体和CREB抑制骨质细胞增殖.

结论:

十二指肠衍生的血清激素作为一种激素,以Lrp5-依赖的方式抑制骨形成.
这项研究建立了一个新的肠骨信号通路,涉及LRp5和血清素.
研究结果表明,针对这一轴的潜在治疗策略可以增强骨质量,并对抗骨质疏松症等骨疾病.

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