Fig. 8
- ID
- ZDB-FIG-221109-38
- Publication
- Zhou et al., 2022 - Dusp6 deficiency attenuates neutrophil-mediated cardiac damage in the acute inflammatory phase of myocardial infarction
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a-c Quantitative RT-PCR (a n = 6 biological independent samples/group), western blot (b) and corresponding quantitative analysis (c n = 4 biological independent samples/group) of Dusp6 mRNA and protein in PMNs isolated from unoperated WT rats and treated with either DMSO, p38 inhibitors (BIRB796 or SB203580), or MEK inhibitors (SL327 or U0126). Both blots were performed in parallel with the same samples. d Representative ChIP assays reveal the interaction between C/EBPβ and the Dusp6 promoter fragment (performed in duplicates using PMNs from 5 normal WT rats each time). Anti-Histone H3 and rabbit IgG were used as positive and negative controls, respectively. e Luciferase reporter activity driven by the Dusp6 promoter with WT sequence (Dusp6-p) or mutations of putative C/EBPβ-binding motifs (mDusp6-p) upon the regulation of C/EBPβ in 293 T cells (performed in duplicates with n = 3/group). The pGL3 empty vector was used as negative control. f Quantitative ChIP assays of C/EBPβ binding to the Dusp6 promoter in WT PMNs treated with either DMSO, p38 inhibitor (BIRB796), or MEK1/2 inhibitor (SL327). 3 replicates were performed with PMNs from at least 5 normal WT rats for each group. All quantitative data shown in this figure are presented as mean values ± SD. One-way ANOVA with Tukey’s multiple comparison test were used to calculate the presented p-values. Source data of a–f are provided in a Source Data File. |