SiXu Chen1, JianQuan Feng2, Hua Zhang2, Min Jia1, Yue Shen1, ZhaoWen Zong3. 1. State Key Laboratory of Trauma, Burn and Combined injury, Department of Trauma Surgery, Daping Hospital, Third Military Medical University, No.10, Changjiang Rd, Yuzhong District, ChongQing 400042, China. 2. Department of Biomedical Sciences, Baylor College of Dentistry, Texas A&M Health Science Center, 2752 Gaston Ave, Dallas, TX 75246, USA. 3. State Key Laboratory of Trauma, Burn and Combined injury, Department of Trauma Surgery, Daping Hospital, Third Military Medical University, No.10, Changjiang Rd, Yuzhong District, ChongQing 400042, China. Electronic address: zongzhaowen@163.com.
Abstract
BACKGROUND CONTEXT: Osterix (Osx) is an important transcriptional factor for bone formation; however, its role in spine development has not been determined. PURPOSE: The goal of the present study is to observe the role of Osx in spine development. STUDY DESIGN/ SETTING: Deletion and overexpression of Osx were achieved in Osx knockout and transgenic mice, respectively, to determine the effect of Osx on spine development. METHODS: With 2.3-kb type I collagen as a promoter, Osx were deleted in mice, and overexpression of Osx was obtained in Osx transgenic mice. Video, X-ray radiology, histology, tartrate-resistant acid phosphatase staining, Safranin O staining, and immunohistochemistry were used to assess the effect of Osx deletion and overexpression on spine development. This study was supported by National Science Foundation of China (81271935) and Foundation of State Key Laboratory of Trauma, Burns and combined injury (SKLZZ SKLZZ201124). No potential conflict of interest to disclose. RESULTS: Overexpression of Osx did not have an obvious effect on spine development, whereas deletion of Osx led to severe spine deformities that included wedged vertebrae, spinal stenosis, and congenital scoliosis. Also, Osx deactivation resulted in shortened vertebrae and excessive bone volume in the vertebrae. TRAP staining showed that activity of osteoclasts decreased in Osx-null mice, and examination with TdT-mediated dUTP nick end labeling revealed that the apoptosis rate at the growth plate decreased significantly in Osx-null mice. Excessive formation of bone was positive for Safranin O staining. CONCLUSIONS: Osx plays an important role in spine development, and its deactivation leads to severe spine deformities.
BACKGROUND CONTEXT: Osterix (Osx) is an important transcriptional factor for bone formation; however, its role in spine development has not been determined. PURPOSE: The goal of the present study is to observe the role of Osx in spine development. STUDY DESIGN/ SETTING: Deletion and overexpression of Osx were achieved in Osx knockout and transgenic mice, respectively, to determine the effect of Osx on spine development. METHODS: With 2.3-kb type I collagen as a promoter, Osx were deleted in mice, and overexpression of Osx was obtained in Osxtransgenic mice. Video, X-ray radiology, histology, tartrate-resistant acid phosphatase staining, Safranin O staining, and immunohistochemistry were used to assess the effect of Osx deletion and overexpression on spine development. This study was supported by National Science Foundation of China (81271935) and Foundation of State Key Laboratory of Trauma, Burns and combined injury (SKLZZ SKLZZ201124). No potential conflict of interest to disclose. RESULTS: Overexpression of Osx did not have an obvious effect on spine development, whereas deletion of Osx led to severe spine deformities that included wedged vertebrae, spinal stenosis, and congenital scoliosis. Also, Osx deactivation resulted in shortened vertebrae and excessive bone volume in the vertebrae. TRAP staining showed that activity of osteoclasts decreased in Osx-null mice, and examination with TdT-mediated dUTP nick end labeling revealed that the apoptosis rate at the growth plate decreased significantly in Osx-null mice. Excessive formation of bone was positive for Safranin O staining. CONCLUSIONS:Osx plays an important role in spine development, and its deactivation leads to severe spine deformities.