Loss of β-Actin Leads to Accelerated Mineralization and Dysregulation of Osteoblast-Differentiation Genes during Osteogenic Reprogramming.

ABSTRACT: Actin plays fundamental roles in both the cytoplasm and the cell nucleus. In the nucleus, β-actin regulates neuronal reprogramming by consolidating a heterochromatin landscape required for transcription of neuronal gene programs, yet it remains unknown whether it has a role in other differentiation models. To explore the potential roles of β-actin in osteogenesis, β-actin wild-type (WT) and β-actin knockout (KO) mouse embryonic fibroblasts (MEFs) are reprogrammed to osteoblast-like cells using small molecules in vitro. It is discovered that loss of β-actin leads to an accelerated mineralization phenotype (hypermineralization), accompanied with enhanced formation of extracellular hydroxyapatite microcrystals, which originate in the mitochondria in the form

SUBMITTER: Gjorgjieva T 

PROVIDER: S-EPMC7709978 | biostudies-literature | 2020 Dec

REPOSITORIES: biostudies-literature