ArticleEuropean journal of histochemistry : EJH2025
Effects of Notch signaling on proliferation, angiogenesis, and adipogenesis of hemangioma-derived stem cells.
Article in European journal of histochemistry : EJH, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- SIRT1 induces FOXO1/autophagy/NCOA4-induced ferroptosis and accelerates the progression of cerebral infarction by inhibiting the E2F1/NOTCH-1/YAP signaling pathway.Scientific reports · 2026Article
- Research Advances in Nanodrugs Targeting Lipid Metabolism Reprogramming for Colorectal Cancer Therapy.International journal of nanomedicine · 2026Review
- Notch signaling pathway and heart development, congenital heart disease, and myocardial regeneration.Frontiers in bioengineering and biotechnology · 2025Review
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Authors and funding
5 authors.
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Abstract
Hemangioma-derived stem cells (Hem-SCs) constitute the cellular basis for adipogenesis during infantile hemangioma (IH) regression, with Notch signaling implicated in this process. To elucidate Notch's role in Hem-SCs biology, we isolated primary Hem-SCs from proliferative-phase IH specimens and validated their stem cell characteristics. Three days post-intervention with the γ-secretase inhibitor DAPT (N‑[N‑(3,5‑difluorophenacetyl)‑L‑alanyl]‑S‑phenylglycine t‑butylester), we assessed Notch and PI3K/AKT signaling dynamics while concurrently measuring vascular endothelial growth factor receptor (VEGFR) protein expression. Cellular proliferation was quantified via CCK-8 assay. During adipogenic differentiation (Day 14), RTqPCR evaluated Notch pathway genes (Notch1, Jagged1, Hes1), while adipogenic commitment was determined through Oil Red O staining and adipocyte-specific gene expression (PPARγ, C/EBPα). We demonstrate that DAPT suppresses Notch and PI3K/AKT signaling in Hem-SCs, concomitantly enhancing cellular proliferation and angiogenesis. Simultaneous analysis of VEGFR expression revealed differential DAPT-mediated regulation: VEGFR1 downregulation with concomitant VEGFR2 upregulation. During adipogenic induction, Notch pathway genes (Notch1, Jagged1, Hes1) were significantly downregulated. DAPT treatment further elevated adipogenic markers (PPARγ, C/EBPα) and lipid accumulation. Crucially, co-administration of the PI3K activator 740Y-P reversed DAPT-induced adipogenesis. Mechanistically, Notch inhibition promotes Hem-SCs proliferation, angiogenesis, and adipocyte differentiation by attenuating PI3K/AKT signaling.
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Registered trials
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