RNA sequencing analysis of WT and Dusp6-/- rat cardiac infiltrated macrophages transcriptomes

Dual-specificity phosphatase 6 (DUSP6), a member of MAPK phosphatase, serves a specific and conserved function on the dephosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) in multiple species. Utilizing a rat strain harboring nonsense mutation of Dusp6, we found that Dusp6 deficiency improves cardiac function by attenuating cardiomyocyte death and fibrosis in acute inflammatory phase after MI. To investigate the effect of DUSP6 on macrophages in acute inflammatory phase of MI, we performed RNA-seq analysis using CD45+HIS36+ macrophages isolated from Dusp6-deficient and WT infarcted LV tissues 72 h after MI by fluorescent activated cell sorting (FACS).双特异性磷酸酶6（Dual-specificity phosphatase 6, DUSP6）作为丝裂原活化蛋白激酶磷酸酶（MAPK phosphatase）家族成员，在多个物种中均对细胞外调节蛋白激酶1/2（extracellular signal-regulated kinase 1/2, ERK1/2）的去磷酸化过程发挥特异性且保守的调控作用。本研究利用携带Dusp6无义突变的大鼠品系，发现Dusp6缺失可通过减轻心肌梗死（Myocardial Infarction, MI）后急性炎症期的心肌细胞死亡与纤维化，改善心脏功能。为探究DUSP6在MI急性炎症期对巨噬细胞的调控效应，我们通过荧光激活细胞分选术（fluorescent activated cell sorting, FACS），从MI造模72小时后的Dusp6缺陷型与野生型（WT）梗死左心室（Left Ventricle, LV）组织中分离得到CD45⁺HIS36⁺巨噬细胞，并对其开展RNA测序（RNA-seq）分析。