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ABSTRACT: Background
Craniofacial malformations, caused by dysregulated neural crest cell (NCC) differentiation, affect approximately one-third of newborns worldwide. Although TGFB3 mutations were recently associated with human coronoid process hypertrophy (CPH) and other craniofacial disorders, the mechanisms by which TGF-β3 regulates NCC fate determination through cell-cell communication remains unknown.Methods
A zebrafish model was used to investigate the impact of tgfb3 on craniofacial cartilage and bone development. Additionally, Tgfb3 was knocked down in neural crest stem cells (NCSCs) in vitro to observe cellular changes and effects on chondrogenic and osteogenic differentiation.Results
Knockdown of tgfb3 in zebrafish resulted in impaired cartilage development and bone
SUBMITTER: Zhang H
PROVIDER: S-EPMC12410403 | biostudies-literature | 2025 Aug
REPOSITORIES: biostudies-literature