β-catenin-dependent High Bone Mass Induced by Loss of APC in Osteoblasts Does Not Require Lrp5 or Lrp6.
β-catenin-dependent High Bone Mass Induced by Loss of APC in Osteoblasts Does Not Require Lrp5 or Lrp6.
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DOI：
10.17912/micropub.biology.001000
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发表时间：
2023
影响因子：
--
通讯作者：
Williams, Bart O
中科院分区：
文献类型：
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作者：
Diegel, Cassandra R;Michalski, Megan N;Williams, Bart O
在没有肿瘤抑制因子APC的情况下，LRP5和LRP6是否需要阻止β-catenin降解尚不清楚，因为细胞培养模型产生了相互矛盾的结果。我们之前已经证实，成骨细胞特异性APC的缺失会导致β-连环蛋白的积累和骨量的增加，而LRP5和LRP6的缺失会减少骨量。我们在这里报道，小鼠成骨细胞中APC、LRP5和LRP6的同时缺失表现了APC成骨细胞特异性敲除。因此，体内成骨细胞APC缺失后β-catenin的稳定和骨量的增加并不依赖于LRP5和LRP6。
The requirement for LRP5 and LRP6 to prevent β-catenin degradation in the absence of the tumor suppressor APC is unclear because cell culture models have yielded conflicting results. We previously established that osteoblast-specific loss of APC causes β-catenin accumulation and increased bone mass, while loss of both LRP5 and LRP6 reduces bone mass. We report here that the simultaneous loss of APC, LRP5, and LRP6 in osteoblasts in mice phenocopies the APC osteoblast-specific knockout. Thus, β-catenin stabilization and increased bone mass after loss of APC in osteoblasts in vivo are not dependent on LRP5 and LRP6.