title: Chondrocyte-specific ablation of Osterix leads to impaired endochondral ossification.
abstract: Osterix (Osx) is an essential transcription factor required for osteoblast differentiation during both intramembranous and endochondral ossification. Endochondral ossification, a process in which bone formation initiates from a cartilage intermediate, is crucial for skeletal development and growth. Osx is expressed in differentiating chondrocytes as well as osteoblasts during mouse development, but its role in chondrocytes has not been well studied. Here, the in vivo function of Osx in chondrocytes was examined in a chondrocyte-specific Osx conditional knockout model using Col2a1-Cre. Chondrocyte-specific Osx deficiency resulted in a weak and bent skeleton which was evident in newborn by radiographic analysis and skeletal preparation. To further understand the skeletal deformity of the chondrocyte-specific Osx conditional knockout, histological analysis was performed on developing long bones during embryogenesis. Hypertrophic chondrocytes were expanded, the formation of bone trabeculae and marrow cavities was remarkably delayed, and subsequent skeletal growth was reduced. The expression of several chondrocyte differentiation markers was reduced, indicating the impairment of chondrocyte differentiation and endochondral ossification in the chondrocyte-specific Osx conditional knockout. Taken together, Osx regulates chondrocyte differentiation and bone growth in growth plate chondrocytes, suggesting an autonomous function of Osx in chondrocytes during endochondral ossification.
authors.affiliation: Department of Molecular Medicine, Cell and Matrix Research Institute, BK21 Medical Education Program for Human Resources, Kyungpook National University School of Medicine, Daegu, Republic of Korea.
authors.forename: Jung-Hoon
authors.initials: JH
authors.lastname: Oh
authors.forename: Seung-Yoon
authors.initials: SY
authors.lastname: Park
authors.forename: Benoit
authors.initials: B
authors.lastname: de Crombrugghe
authors.forename: Jung-Eun
authors.initials: JE
authors.lastname: Kim
mesh_terms: D000818:Animals; D001842:Bone and Bones / Q000002:abnormalities*; D019902:Chondrocytes / Q000378:metabolism*; D020219:Chondrogenesis / Q000235:genetics*; D017353:Gene Deletion; D006811:Humerus / Q000196:embryology / Q000378:metabolism; D051379:Mice; D018345:Mice, Knockout; D010010:Osteoclasts / Q000378:metabolism; D010012:Osteogenesis / Q000235:genetics*; D000076182:Sp7 Transcription Factor; D014157:Transcription Factors / Q000235:genetics / Q000502:physiology*
chemical_list: D000076182:Sp7 Transcription Factor; C479466:Sp7 protein, mouse; D014157:Transcription Factors