Differenatiation of mRNA expression in PTX3-depleted macrophages

PTX3, as the long member of the pentraxin family, is produced mainly by dendritic cells, macrophages, and endothelial cells in response to inflammation. Growing amount of studies suggest that PTX3 can exert potential contradictory roles in inflammation regulation, antimicrobial resistance, and disease pathogenesis, depending on the tissue context, cellular source, and levels of production. To characterize the potential involvement of PTX3 in macrophage function, transcriptome sequencing (RNA-seq) was performed in human THP1-derived macrophages with PTX3 depletion. Notably,genes enrichment in PI3K/AKT signaling , JAK/STAT signaling and autophagy pathway were observed in PTX3 deficiency macrophages. This study highlights the critical roles of PTX3 on regulation macrophages homeostasis. Overall design: The mRNA profiles of WT and PTX3-depleted macrophages under IL-4 stimulation. Three independent experiments were performed at each treatment.

PTX3作为五聚素家族（pentraxin family）的长链成员，主要由树突状细胞、巨噬细胞及内皮细胞在炎症应答过程中产生。越来越多的研究表明，PTX3在炎症调控、抗菌防御及疾病发病机制中可发挥潜在的双向调控作用，其具体功能依赖于组织微环境、细胞来源以及表达水平。为明确PTX3在巨噬细胞功能中的潜在调控作用，本研究对经PTX3敲低的人源THP1巨噬细胞开展了转录组测序（RNA-seq）。值得注意的是，在PTX3缺陷巨噬细胞中，可观察到PI3K/AKT信号通路、JAK/STAT信号通路及自噬通路相关基因的富集特征。本研究揭示了PTX3在调控巨噬细胞稳态中的关键功能。实验设计概要：白细胞介素4（IL-4）刺激条件下，野生型（WT）与PTX3敲低巨噬细胞的mRNA表达谱。每组处理均设置3次独立生物学重复。