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Article Abstract
Objectives: The pathogenesis of mandibular condylar hypoplasia has not been fully understood. Our previous studies provided evidence that Gli1 osteogenic progenitors contribute to condylar development. This study aimed to investigate the role of YAP in Gli1 cells during condylar development.
Methods: We generated Gli1-Cre;Yap mice, in which tamoxifen (TMX) was used to induce the deletion of Yap in Gli1 cells. CHIR injection was to activate β-catenin signaling. Microscopic photography, Micro-CT, hematoxylin-eosin (H&E) staining, immunofluorescence (IF) staining, Real-time quantitative polymerase chain reaction (RT-qPCR), tartrate-resistant acid phosphatase (TRAP) staining and calcein-alizarin red double labeling were conducted for analyses. Chromatin immunoprecipitation (ChIP) assay was used to investigate the molecular mechanism involved.
Results: YAP co-localized with mandibular condylar Gli1 osteogenic progenitors. After induction, Gli1-Cre;Yap mice suffered from condylar hypoplasia characterized by reduced bone mass and impaired osteogenesis due to decreased cell proliferation. ChIP-qPCR analysis, RT-qPCR analysis, and immunofluorescence staining further proved that YAP could directly regulate the expression of β-catenin. Functionally, pharmacological activation of β-catenin signaling successfully alleviated condylar hypoplasia in Gli1-Cre;Yap mice.
Conclusions: Our study demonstrated that the YAP/β-catenin axis mediated osteogenesis in Gli1 osteogenic progenitors during condylar development, which may provide a potential target for the treatment of condylar hypoplasia.
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| http://dx.doi.org/10.1111/odi.70006 | DOI Listing |
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