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• W4311566298 abstract "Abstract Fragile X Messenger Ribonucleoprotein 1 (FMR1) gene premutations lead to fragile X syndrome, cognitive disorders, and, in some individuals, scoliosis and craniofacial abnormalities. Four-month-old male FMR1 -deficient mice exhibit a mild increase in cortical and cancellous femoral bone mass. However, consequences of FMR1-deficiency in bone of young and aged and of male and female mice and the cellular basis of the skeletal phenotype remain unknown. We found that FMR1-deficiency results in improved bone properties with higher bone mineral density in both sexes and in 2- and 9-month-old mice. But cancellous bone mass is higher only in females, whereas, cortical bone mass is higher in 2- and 9-mo males, but higher in 2- and lower in 9-month-old female FMR1-deficient mice. Further, male bones show higher biomechanical properties in 2-month-old, and females at both ages. FMR1-deficiency increases osteoblast number, mineralization, and bone formation and osteocyte dendricity and gene expression in vivo , ex vivo , and in vitro , without affecting osteoclasts in vivo or ex vivo . Thus, FMR1 is a novel osteoblast/osteocyte differentiation inhibitor, and its absence leads to age-, site- and sex-dependent higher bone mass and strength." @default.
• W4311566298 created "2022-12-27" @default.
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• W4311566298 date "2022-12-15" @default.
• W4311566298 modified "2023-10-14" @default.
• W4311566298 title "Fragile X Messenger Ribonucleoprotein 1 (FMR1), a novel inhibitor of osteoblast/osteocyte differentiation, regulates bone formation, mass, and strength in young and aged male and female mice." @default.
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• W4311566298 doi "https://doi.org/10.21203/rs.3.rs-2338908/v1" @default.
• W4311566298 hasPublicationYear "2022" @default.
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