Gain- and loss-of-function of Engrailed 1 in mesenchymal stromal cells affect their potential to differentiate into osteoblasts and to repair bone tissue.
Calixto RD., de Oliveira FS., Almeida ALG., Rosa AL., Beloti MM.
Animal Study, published in Int J Biol Macromol (2026) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Int J Biol Macromol (2026)
- Country
- Netherlands
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 42448202
- DOI
- 10.1016/j.ijbiomac.2026.153544
Abstract (original English)
Engrailed 1 (En1) is a developmental transcription factor associated with skeletal formation; however, its functional role in mesenchymal stromal cell (MSC)-driven osteogenesis remains poorly understood. Here, we demonstrated that En1 is a critical regulator of adipose-derived MSCs differentiation into osteoblasts and bone repair induced by cell therapy using this MSC population. Using CRISPR-Cas9-based gain- and loss-of-function approaches in immortalized MSCs, we showed that En1 overexpression robustly enhanced osteoblastic differentiation, increasing RUNX2 protein level, alkaline phosphatase activity, and extracellular matrix mineralization, whereas En1 silencing produced the opposite effects. In a murine calvarial defect model, En1-overexpressing MSCs significantly improved bone formation and microarchitectural parameters, whereas En1-deficient MSCs impaired bone repair. Notably, temporal gene expression analyses revealed a dynamic, stage-dependent role for En1 during osteogenesis, consistent with the coordinated regulation of early commitment and later maturation. These effects were supported by consistent molecular, phenotypic, and in vivo outcomes. Collectively, our findings establish En1 as a key positive regulator of MSC-mediated osteogenesis and identify this transcription factor as a promising target for cell- and gene-based therapeutic strategies aimed at enhancing
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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