Summarized RNA-seq data
Description
Our research hypothesizes that Notch1 plays a critical role in regulating macrophage polarization and inflammatory pathways in the CLP-induced sepsis model. This transcriptomic dataset is derived from peritoneal macrophages of wild-type (WT) mice and macrophage-specific Notch1 conditional knockout (Notch1 CKO) mice under septic conditions, revealing the regulatory mechanisms of Notch1 in macrophage function. The data demonstrate significant gene expression differences between the two groups of macrophages, showing that Notch1 CKO markedly alters the transcriptomic profile of macrophages, particularly in pathways associated with M1 polarization and inflammation. Specifically, the expression of inflammatory cytokines (e.g., IL-1β, TNF-α) is significantly reduced in Notch1 CKO macrophages, accompanied by the suppression of key signaling pathways such as β-Catenin and NF-κB. These findings highlight the role of Notch1 in promoting M1 polarization and inflammatory responses. Additionally, increased expression of genes associated with an anti-inflammatory phenotype was observed following Notch1 deletion, indicating its pivotal role in maintaining the balance of macrophage polarization. The data were obtained using transcriptomic sequencing. Peritoneal macrophages were isolated from septic mice subjected to CLP, and RNA was extracted for high-throughput sequencing. The mice included two genotypes (WT and Notch1 CKO) and were sampled at the same time point post-CLP induction. Sequencing data underwent quality control, mapping to the mouse reference genome, differential gene expression analysis, and pathway enrichment using tools such as DESeq2 and GSEA. These data underscore the critical role of Notch1 in regulating the transcriptional programs of macrophages in a sepsis model and reveal its molecular mechanisms in promoting M1 polarization through the β-Catenin and NF-κB signaling pathways. The findings provide valuable insights into the potential of targeting Notch1 as a therapeutic strategy for sepsis and other inflammation-related diseases. Researchers can utilize this dataset to investigate gene regulatory networks in macrophages and Notch1-dependent inflammatory mechanisms, as well as validate or compare findings in studies of immune and inflammatory diseases. The data are organized in a standardized format to facilitate reproducibility and further analysis.