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The PLAGL1-KLF4-IRX5 axis promotes the osteogenesis of periosteal progenitors during mandible regeneration [CUT＆tag-Seq]

ABSTRACT: Transcription factor (TF) networks are pivotal in regulating the fate of stem/progenitor cells. However, the intricate regulatory mechanisms mediated by key TFs in adult periosteal stem/progenitor cells (PSPCs) remain poorly understood, hindering the development of targeted therapies for craniofacial bone regeneration. Here, we show that the imprinted TF PLAGL1 is critical for osteoblast differentiation in PSPCs. Furthermore, we identify that PLAGL1 transcriptionally activates TF Irx5 in collaboration with TF KLF4, which, in turn, induces the expression of downstream osteogenic genes.

ORGANISM(S): Mus musculus

PROVIDER: GSE298229 | GEO | 2026/04/06

REPOSITORIES: GEO

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The PLAGL1-KLF4-IRX5 axis promotes the osteogenesis of periosteal progenitors during mandible regeneration [ATAC-seq]

Project description:Transcription factor (TF) networks are pivotal in regulating the fate of stem/progenitor cells. However, the intricate regulatory mechanisms mediated by key TFs in adult periosteal stem/progenitor cells (PSPCs) remain poorly understood, hindering the development of targeted therapies for craniofacial bone regeneration. Here, we show that the imprinted TF PLAGL1 is critical for osteoblast differentiation in PSPCs. Furthermore, we identify that PLAGL1 transcriptionally activates TF Irx5 in collaboration with TF KLF4, which, in turn, induces the expression of downstream osteogenic genes.

2026-04-06 | GSE298228 | GEO

The PLAGL1-KLF4-IRX5 axis promotes the osteogenesis of periosteal progenitors during mandible regeneration [ATAC-seq]

Project description:The PLAGL1-KLF4-IRX5 axis promotes the osteogenesis of periosteal progenitors during mandible regeneration [ATAC-seq]

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The PLAGL1-KLF4-IRX5 axis promotes the osteogenesis of periosteal progenitors during mandible regeneration [CUT＆tag-Seq]

Project description:The PLAGL1-KLF4-IRX5 axis promotes the osteogenesis of periosteal progenitors during mandible regeneration [CUT＆tag-Seq]

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Piezo1 balances the osteogenic-tenogenic plasticity of periosteal progenitor cells through the YAP pathway

Project description:The extremity tendons and bones are derived from limb bud mesenchyme, which eventually become cells of different tissues. Despite their common origin, it was widely believed that tenocytes and skeletal cells are distinct lineages without interconversion. However, we found that periosteal skeletal progenitor cells could transform between osteogenic and tenogenic commitment. SCX can label the periosteal progenitor cell population. Loss of Piezo1 arrests the periosteal progenitor cells in a progenitor state. Piezo1 deficiency leads to upregulation of Scx expression due to the inhibited YAP nuclear localization. Loss of Piezo1 showed increased tenogenic marker genes and decreased osteogenic marker genes. The periosteal progenitor cells can regenerate the injured tendon more robustly when Piezo1 is absent. Taken together, our data reveal that periosteal SCX+ progenitor cells compromise the osteogenic ability and acquire the tenocyte-biased lineage commitment after loss of Piezo1, providing a strategy to modulate the periosteal progenitor cells for tissue regeneration.

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Project description:Aging profoundly impacts bone homeostasis and regeneration, yet the cellular and molecular mechanisms underlying periosteal aging remain poorly understood. Using single-cell RNA sequencing, we profiled the periosteum of 3-, 9-, and 18-month-old mice, revealing age-related shifts in progenitor, neutrophil, and macrophage subpopulations. Aging reduced mesenchymal cell populations and impaired osteogenic potential, disrupting periosteal homeostasis. Periosteal progenitor subsets exhibited distinct aging trajectories: Dpt⁺ fibrous-layer cells undergoing early senescence, while Postn⁺ progenitors showed osteogenic decline. Aging also shifted immune profiles, increasing inflammatory Cd38hi macrophages and dysfunctional Nlrp3hi neutrophils, further disrupting bone homeostasis. Notably, aged progenitor cells upregulated CSF1 and CXCL signaling, driving macrophage and neutrophil infiltration, exacerbating bone loss. Our findings provide a comprehensive periosteal aging atlas, highlighting disrupted progenitor-immune crosstalk as a key driver of bone homeostasis imbalance and impaired regeneration, offering potential therapeutic targets for age-related bone disorders.

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Project description:Periosteal expansion is a key process in the early stages of bone fracture repair. The periosteum is typically quiescent, but upon fracture it expands, periosteal cells proliferate and contribute to the formation of a cartilaginous callus . The early expansion of the periosteum is tightly regulated at the transcriptional level. However, the molecular mechanisms behind periosteal expansion are unknown. Here, we show that Yes-Associated Protein (YAP) and transcriptional co-activator with PDZ-binding motif (TAZ) mediate periosteal expansion and periosteal cell proliferation. Bone fracture results in increased numbers of YAP-expressing periosteal cells. Deletion of YAP from Osterix (Osx) expressing periosteal cells impairs early periosteal expansion. Mechanistically, YAP regulates both cell intrinsic and extrinsic transcriptional programs that allow for periosteal expansion. Specifically, we identified Bmp4 as a cell extrinsic factor regulated by YAP, that rescues the impairment of periosteal expansion upon YAP deletion. Together, these data establish YAP mediated molecular mechanisms that allow for periosteal expansion in the early stages of fracture repair.

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