Basic & Clinical Medicine ›› 2020, Vol. 40 ›› Issue (3): 294-298.

• Original Articles • Previous Articles     Next Articles

Regulation of co-transcription factor CITED1 in mouse bone metabolism

QIU Yi-yan1,2*, ZHENG Yu-cheng1, GUO Wei-zhuang1, ZHOU Wen-yu1, YAN Bin1, YANG Xin-jian1   

  1. 1. Department of Orthopedics, the Second People's Hospital of Shenzhen, Shenzhen 518000;
    2. Department of Orthopedics, the Third Affiliated Hospital of Southem Medical University, Guangzhou 510630, China
  • Received:2019-05-07 Revised:2019-11-04 Online:2020-03-05 Published:2020-03-02
  • Contact: *

Abstract: Objective To study the regulation of CITED1 in the mice bone metabolism, including osteogenesis/osteoclast balance in vivo to provide a theoretical basis for the treatment of osteoporosis. Methods Bone phenotypes such as femur length, bone mass, bone cortex and bone cancellous thickness of KO mice were measured by micro CT. Hematological related parameters of bone metabolism were determined by ELISA. RT-qPCR was used to detect the expression of bone marker genes to explore the causes of bone metabolism changes after CITED1 gene knockout. Results The expression of CITED1 was low in KO mice, indicating a successful CITED1 knockout. Femoral length, bone mass, bone cortex and bone cancellous thickness were significantly higher in KO mice than those in WT mice. The concentration of type I procollagen peptide (P1NP), osteocalcin (OC) and bone alkaline phosphatase (BALP) in serum of KO mice was significantly higher than those of WT mice, while the concentration of tartaric acid phosphatase (TRAP) was significantly lower. The expression of OC and BALP in KO mice was significantly higher than that in WT mice(P<0.001). At the same time the expression of TRAP in KO mice was signifi- cantly lower(P<0.05). Conclusions CITED1 knockout can up-regulate the expression of OC and BALP, and down-regulate the expression of TRAP for promoting bone formation and inhibiting bone resorption.

Key words: co-transcription factor CITED1, osteoporosis, parathyroid hormone, bone metabolism

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