Project description:By utilizing a series of specific modulating M2 macrophages polarization models, 3872 up-regulated and 3091 down-regulated genes were found during the polarization process.
Project description:By utilizing a series of specific modulating M2 macrophages polarization models, 1556 up-regulated and 953 down-regulated genes were found during the polarization process.
Project description:To determine lncRNAs transcribed during the polarization of macrophages, we have employed whole genome microarray expression profiling as a discovery platform to identify lncRNAs expression in mouse primary bone marrow derived macrophages (BMDMs) treated with M1 (lipopolysaccharide, LPS) and M2 (IL-4) stimulators.
Project description:Microglia M2 polarization plays an important role in the regulation of neuroinflammation, but the molecular mechanisms behind it remain unclear. This study researched the expression profiles of mRNAs in microglia M2 polarization cell model.
Project description:Microglia M2 polarization plays an important role in the regulation of neuroinflammation, but the molecular mechanisms behind it remain unclear. This study researched the expression profiles of circRNAs in microglia M2 polarization cell model.
Project description:Despite significant advancements in cancer immunotherapy, many patients continue to respond poorly. Novel therapeutic strategies and drugs are urgently needed. Here, we found that CYP2E1 is significantly upregulated in M2 macrophages. The CYP2E1 inhibitor, Q11, could inhibit M2 macrophage polarization, while CYP2E1 overexpression could promote it. Increased levels of CYP2E1 and M2 macrophages in the tumor microenvironment of HCC patients correlate with poor prognosis. Q11 could inhibit tumor cells by targeting M2 macrophages rather than directly attacking tumor cells. Both Q11 and Cyp2e1 knockout could effectively suppress tumor growth. Q11 reduces the production of CYP2E1 metabolites (±)9(10)-DiHOME and (±)12(13)-DiHOME, thus attenuating PPARγ activation and M2 macrophage polarization. In summary, our findings suggest that Q11 could suppress M2 macrophage polarization by modulating the CYP2E1/(±)9(10)-DiHOME or (±)12(13)-DiHOME/PPARγ axis, indicating that CYP2E1 inhibition may be a novel therapeutic strategy for HCC and positioning Q11 as a promising therapeutic agent.
Project description:Exercise benefits M2 macrophage polarization, energy homeostasis and protects against obesity partially through exercise-induced circulating factors. Here, by unbiased quantitative proteomics on serum samples from sedentary and exercised mice, we identify parvalbumin as a circulating factor suppressed by exercise. Parvalbumin functions as a non-competitive CSF1R antagonist to inhibit M2 macrophage activation and energy expenditure in adipose tissue. More importantly, serum concentrations of parvalbumin positively correlate with obesity in mouse and human, while treating mice with a recombinant parvalbumin blocker prevents its interaction with CSF1R and promotes M2 macrophage polarization and ameliorates diet-induced obesity. Thus, although further studies are required to assess the significance of parvalbumin in mediating the effects of exercise, our results implicate parvalbumin as a potential therapeutic strategy against obesity.
Project description:BRD4 inhibition suppressed M2 macrophage polarization. Particularly, we deeply investigated the underlying molecular mechanism of how BRD4 regulate M2 genes expression. And finished this RNA-seq
Project description:Polarization of macrophages to M1 or M2 cells is important for mounting responses against bacterial and helminth infection respectively. Jumonji domain containing 3 (JMJD3), a histone 3 K27 demethylase, has been implicated in the activation of macrophages. Here we show that JMJD3 is essential for M2 macrophage polarization to helminth infection and chitin, though JMJD3 is dispensable for M1 responses. Furthermore, Jmjd3 is critical for proper bone marrow macrophage differentiation in a demethylase activity-dependent manner. Jmjd3 deficiency affected trimethylation of H3K27 in only a limited numbers of genes. Among them, we identified Irf4 as the target transcription factor critical for controlling M2 macrophage polarization. Collectively, these results show that JMJD3-mediated H3K27 demethylation is critical for regulating M2 macrophage development leading to anti-helminth host responses. This SuperSeries is composed of the SubSeries listed below.