Wnt-mediated reciprocal regulation between cartilage and bone development during endochondral ossification.

Cheng Lu, Yong Wan, Jingjing Cao, Xuming Zhu, Jian Yu, Rujiang Zhou, Yiyun Yao, Lingling Zhang, Haixia Zhao, Hanjun Li, Jianzhi Zhao, Lin He, Gang Ma, Xiao Yang, Zhengju Yao, Xizhi Guo

Research output: Contribution to journalArticlepeer-review

Abstract

The role of Wnt signaling is extensively studied in skeletal development and postnatal bone remodeling, mostly based on the genetic approaches of β-catenin manipulation. However, given their independent function, a requirement for β-catenin is not the same as that for Wnt. Here, we investigated the effect of Wnt proteins in both tissues through generating cartilage- or bone-specific Wls null mice, respectively. Depletion of Wls by Col2-Cre, which would block Wnt secretion in the chondrocytes and perichondrium, delayed chondrocyte hypertrophy in the growth plate and impaired perichondrial osteogenesis. Loss of Wls in chondrocytes also disturbed the proliferating chondrocyte morphology and division orientation, which was similar to the defect observed in Wnt5a null mice. On the other hand, inactivation of Wls in osteoblasts by Col1-Cre resulted in a shorter hypertrophic zone and an increase of TRAP positive cell number in the chondro-osseous junction of growth plate, coupled with a decrease in bone mass. Taken together, our studies reveal that Wnt proteins not only modulate differentiation and cellular communication within populations of chondrocytes, but also mediate the cross regulation between the chondrocytes and osteoblasts in growth plate.

Original languageEnglish (US)
Pages (from-to)566-574
Number of pages9
JournalBone
Volume53
Issue number2
DOIs
StatePublished - Apr 2013
Externally publishedYes

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