Loss of Hdac4 in osteoprogenitors impairs postnatal trabecular and cortical bone formation, resulting in a dwarfism and osteopenia phenotype in mice.

ABSTRACT: HDAC4 is a class II histone deacetylation protein with a well-characterized role in chondrocyte differentiation and skeletal development, and dysregulated expression or haploinsufficiency of Hdac4 leads to skeletal formation and malformation disorders. The early lethality of Hdac4 ablation mice hindered further investigation of its role in postnatal bone growth and development. Therefore, this study aims to investigate the significant role of Hdac4 in postnatal endochondral bone development using two mouse models with conditional deletion of Hdac4 in Sp7-expressing osteoprogenitors or chondrocytes and monitored postnatal bone development. The phenotype of Acan-Cre^ERT2; Hdac4^fl/fl mice largely resembled that of conventional Hdac4^-/- mice. But phenotypic char

SUBMITTER: Wang Y 

PROVIDER: S-EPMC11664417 | biostudies-literature | 2024 Oct

REPOSITORIES: biostudies-literature