Fig. 3: NAT10 knockdown inhibits keratinocyte migration through impairing IL-6 expression.
From: N-acetyltransferase 10 promotes cutaneous wound repair via the NF-κB-IL-6 axis
A The schematic diagram described the induction of cytokines, chemokines, MMPs and growth factors expression by scratch-induced wound at different time points. B The heat map showing the production of cytokines, chemokines, MMPs and growth factors at serial time points in keratinocyte cells post scratching. C qPCR analysis of the expression of several key cytokines in HaCaT cells treated with control or NAT10 siRNAs in the scratch-wounded model (n = 3 for each group). n.s., no significance. D Immunoblotting analysis showing level of phosphorylated STAT3 in HaCaT cells treated with control or NAT10 siRNAs in the wound healing model. E, F Representative images (E) and related quantitative analysis showing the trans-well assays (lasting for 24 h) of HaCaT cells with or without NAT10 knockdown in the presence of absence of rIL-6. rIL-6, exogenous recombinant human IL-6 (n = 5 for each group). Scale bars, 50 μm. G, H Representative images and related quantitative analysis showing the in vitro wound healing assay of HaCaT cells (lasting for 16 h) treated with NAT10 siRNA or rIL-6 (n = 3 for each group). Scale bars, 50 μm. I Immunoblot analysis of phosphorylated STAT3 expression in HaCaT cells treated with NAT10 siRNAs and rIL-6 or not. Data are represented as mean ± SEM. * P < 0.05, ** P < 0.01, determined by Student’s t test.
