title: Wnt-mediated reciprocal regulation between cartilage and bone development during endochondral ossification.
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.
authors.affiliation: Bio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders (Ministry of Education), Shanghai Jiao Tong University, Shanghai 200240, China.
authors.forename: Cheng
authors.initials: C
authors.lastname: Lu
authors.forename: Yong
authors.initials: Y
authors.lastname: Wan
authors.forename: Jingjing
authors.initials: J
authors.lastname: Cao
authors.forename: Xuming
authors.initials: X
authors.lastname: Zhu
authors.forename: Jian
authors.initials: J
authors.lastname: Yu
authors.forename: Rujiang
authors.initials: R
authors.lastname: Zhou
authors.forename: Yiyun
authors.initials: Y
authors.lastname: Yao
authors.forename: Lingling
authors.initials: L
authors.lastname: Zhang
authors.forename: Haixia
authors.initials: H
authors.lastname: Zhao
authors.forename: Hanjun
authors.initials: H
authors.lastname: Li
authors.forename: Jianzhi
authors.initials: J
authors.lastname: Zhao
authors.forename: Lin
authors.initials: L
authors.lastname: He
authors.forename: Gang
authors.initials: G
authors.lastname: Ma
authors.forename: Xiao
authors.initials: X
authors.lastname: Yang
authors.forename: Zhengju
authors.initials: Z
authors.lastname: Yao
authors.forename: Xizhi
authors.initials: X
authors.lastname: Guo
mesh_terms: D000818:Animals; D001846:Bone Development / Q000235:genetics / Q000502:physiology*; D002356:Cartilage / Q000254:growth & development* / Q000378:metabolism*; D005260:Female; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D047908:Intracellular Signaling Peptides and Proteins / Q000235:genetics / Q000378:metabolism; D008297:Male; D051379:Mice; D043562:Receptors, G-Protein-Coupled; D051153:Wnt Proteins / Q000235:genetics / Q000378:metabolism*
chemical_list: C545200:Gpr177 protein, mouse; D047908:Intracellular Signaling Peptides and Proteins; D043562:Receptors, G-Protein-Coupled; D051153:Wnt Proteins