Research On The Roles Of PIP5K1C In Regulation Of Bone Homeostasis

Bone is one of the largest organs of human body and can support and bear pressure.Osteoporosis and osteoarthritis are a relatively high incidence rate in the elderly population in China,and seriously affect the quality of life and safety of patients.At present,with the aging of the population in China,the treatment methods for osteoporosis and other bone metabolic diseases are limited.Therefore,the study of the phenotype and molecular mechanism of osteoporosis and other bone metabolic diseases may provide new treatment methods and means for patients.In this study,we investigated the regulation mechanism of pip5k1 c on bone homeostasis in mice with pip5k1 c knockout.In the micro CT analysis of bone mass of knockout mice,it was found that the bone mass of mice was decreased when the cells knocked out pip5k1 c.The expression of osteogenic factor and adipogenic factor in bone marrow mesenchymal stem cells decreased,and the number of cells differentiated into osteoblast precursor cells decreased.The number of bone marrow mesenchymal stem cells in bone marrow decreased,and the number of osteoblast colony forming mineralized nodules also decreased.The results showed that the decrease of bone mass was due to the decrease of bone formation activity in knockout mice.At the same time,in knockout mice,immunohistochemical staining showed that the number of osteoclasts decreased,and the expression of RANKL in bone tissue also decreased.The detection of factors in serum of knockout mice also showed that the content of factors related to osteoclast activity was significantly reduced compared with the control group.The decrease in the number of osteoclasts may be due to the influence of bone marrow mesenchymal stem cells on the differentiation ability of osteoclast precursor cells.Therefore,to sum up,after pip5k1 c knockout,bone formation and bone resorption activities in the bone tissue of mice were weakened,and the bone formation ability was more affected,resulting in the decrease of bone mass in mice.