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Importantly, PPAR-γ activity is impaired in wound macrophages of diabetic mice and humans, and topical application of PPAR-γ agonists induced an M2- like wound macrophage phenotype and improved healing in diabetic mice [42].
In a recent study, wound macrophages from diabetic db/db mice exhibited a more M1- like phenotype than those from non-diabetic mice both at days 4 and 7 post-injury [47].
Similar results were produced using pre-diabetic high fat diet (HFD)- fed mice, as wound macrophages exhibited a more M1-like phenotype on days 3 and 7 post-injury, and this phenotype difference was trans- mitted by bone marrow transfer from HFD or lean donor mice to lean recipient mice [48].
An epigenetic mechanism may explain the intrinsic programming of diabetic macrophages, as repressive histone methyla- tion is decreased at the promoter of the IL-12 gene in bone marrow pro- genitors, resulting in increased IL-12 production in progeny wound macrophages [48].
healing-associated wound macrophage phenotype and improves healing in type 2 diabetes, Diabetes 62 (7) (2013) 2579-2587.
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