Low-dose G-CSF improves fat graft retention by mobilizing endogenous stem cells and inducing angiogenesis, whereas high-dose G-CSF inhibits adipogenesis with prolonged inflammation and severe fibrosis.
Cai J., Li B., Liu K., Feng J., Gao K., Lu F.
Animal Study on Hip, published in Biochem Biophys Res Commun (2017) — 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
- Biochem Biophys Res Commun (2017)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 28756227
- DOI
- 10.1016/j.bbrc.2017.07.147
- Citations
- 25
Abstract (original English)
Hematopoietic stem cells (HSCs) promote fat graft survival by modulating its revascularization. The authors hypothesize that mobilization of HSCs by G-CSF will improve fat graft survival. Hence, we evaluated the effect of different doses of G-CSF on fat grafting. Male 8-week-old C57 mice received high-dose G-CSF (100 μg/kg), low-dose G-CSF (10 μg/kg), and PBS (control) intraperitoneally for 7 consecutive days right after autologous fat grafting. Grafted fat was harvested at 1, 4, and 12 weeks for examination. The low-dose G-CSF, high-dose G-CSF, and control groups had retention rates of 73.6% ± 3.1%, 51.6% ± 4.4%, and 44.5% ± 4.0%, respectively, at 12 weeks (low-dose G-CSF versus control and low-dose G-CSF versus high-dose G-CSF, both p < 0.05; no significant difference between high-dose G-CSF and control group). Both doses of G-CSF successfully mobilized HSCs into circulation and upregulated the level of blood-derived stem cells in fat grafts, contributing to improved angiogenesis. However, high-dose G-CSF caused a prolonged macrophage infiltration and elevated level of inflammation (IL-6 and TNF-α), which led to severe fibrosis and impaired adipogenesis (downregulated expression of PPAR-γ and CEBP-α). Low-dose G-CSF treatment successfully improved fat graft survival by mobilizing HSCs and inducing angiogenesis. However, high-dose G-CSF prolonged inflammation and caused severe
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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