Upregulation of MicroRNA-125b Leads to the Resistance to Inflammatory Injury in Endothelial Progenitor Cells

Figures

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  Figure 1. miR-125b overexpression in EPCs preserved its migration and adhesion function after TNF-α treatment. EPCs were transfected with miR-125b mimic and negative control mimic for 24 h. (a) The level of miR125b measured by qRT-PCR (b). EPC migration and adhesion measured after transfection. Representative (c) and quantification (d) of the migratory activity of EPCs. Representative (e) and quantification (f) of DiI-labeled EPC adhesion to HUVECs with TNF-α activation (scale bar = 100 μm, ∗p < 0.05 vs. NC mimic with TNF-α treatment, n = 5).

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  Figure 2. Upregulation of miR-125b in EPCs attenuated the expression of proinflammatory factors and ameliorated the TNF-α-induced cell apoptosis. EPCs were treated with TNF-α (10 ng/mL) for 1 h after transfection. The mRNA levels of proinflammatory factors (TNF-α, IL-1β, and IL-6) were measured by qRT-PCR (a). Cell apoptosis was determined by flow cytometry using annexin V staining (b). The activation of caspase3 was analyzed by western blotting. Representative (c) and quantification (d) of caspase3 level (normalized to β-actin). The activation of NF-κB was determined by the level of p-p65 in EPCs using western blotting. Representative (e) and quantification (f) of p-p65 level (normalized to p65) (∗p < 0.05 vs. NC mimic with TNF-α treatment, n = 5).

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  Figure 3. miR-125b overexpression enhanced the EPC-mediated neovascularization and cardiac function recovery in the ischemic hearts. The cardiac function was assessed by echocardiography at baseline and after MI (28 days). Representative (a) and quantification (b) of echocardiography analyses. EPC-mediated neovascularization in the ischemic hearts analyzed by CD31 staining (GFP) (c) and capillary density quantified (d) (scale bar = 100 μm, ∗p < 0.05 vs. NC mimic, n = 5).