TY - JOUR
T1 - Wnt-mediated reciprocal regulation between cartilage and bone development during endochondral ossification.
AU - Lu, Cheng
AU - Wan, Yong
AU - Cao, Jingjing
AU - Zhu, Xuming
AU - Yu, Jian
AU - Zhou, Rujiang
AU - Yao, Yiyun
AU - Zhang, Lingling
AU - Zhao, Haixia
AU - Li, Hanjun
AU - Zhao, Jianzhi
AU - He, Lin
AU - Ma, Gang
AU - Yang, Xiao
AU - Yao, Zhengju
AU - Guo, Xizhi
PY - 2013/4
Y1 - 2013/4
N2 - 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.
AB - 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.
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U2 - 10.1016/j.bone.2012.12.016
DO - 10.1016/j.bone.2012.12.016
M3 - Article
C2 - 23274346
AN - SCOPUS:84891669117
SN - 8756-3282
VL - 53
SP - 566
EP - 574
JO - Bone
JF - Bone
IS - 2
ER -