Myosin 1b Inhibits the Phenotype of HemECs to Affect the Progression of Infantile Hemangiomas
Li N., Gong X., Cao Z., Li Z., Wang L., Huo R.
Animal Study, published in Clin Cosmet Investig Dermatol (2025) — 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
- Clin Cosmet Investig Dermatol (2025)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 40296866
- PMCID
- PMC12036681
- DOI
- 10.2147/ccid.s517750
Abstract (original English)
Purpose To investigate the role of myosin 1b (Myo1b) in infantile hemangiomas (IHs). Patients and methods The expression of Myo1b in IHs and normal skin tissues was evaluated using immunohistochemical techniques. Expression of Myo1b in hemangioma endothelial cells (HemECs) was detected using quantitative real-time polymerase chain reaction and Western blotting techniques. The effects of Myo1b on cell proliferation, invasion, tube formation and other biological characteristics were analyzed. A mouse model was established to observe the inhibitory effects of Myo1b in vivo. Protein expression of peroxisome proliferator-activated receptor-gamma (PPARγ) and glucose transporter 1 protein (Glut-1) in a Myo1b knockdown HemECs was detected using Western blot. Results Myo1b was highly expressed in the proliferative stage of IHs, and promoted proliferation, invasion, and angiogenesis in vitro. Mouse models further demonstrated that Myo1b inhibited proliferation and angiogenesis of IHs. Knockdown of Myo1b inhibited Glut-1 activity, promoted expression of PPARγ transcription factor. Conclusion Myo1b has a pro-tumor effect on IHs, knockdown of Myo1b facilitated progression of the proliferating to involution phase of IHs. Therefore, Myo1b is expected to serve as a new target for the treatment of IHs.
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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