Project description:In response to microenvironmental signals macrophages undergo different activation, indicated as classic/M1 and alternative/M2 polarization. C-Myc transcription factor could be an essential player in M2 polarization. Functional relevance of c-Myc in M2 macrophage biology is investigated by evaluating the effect of 100-58F4, on the transcriptional profile induced on human macrophages by IL-4. Human monocytes were obtained from normal donor buffy coats by two-step gradient centrifugation using Ficoll (Biochrom) and Percoll (Amersham). Non-adherent cells were discarded, and the purified monocytes were incubated for 7 days in RPMI 1640 (Biochom) supplemented with 10% FCS (HyClone) and 100 ng/mL M-CSF to obtain resting macrophages. Macrophage polarization was obtained by removing the culture medium and culturing cells in RPMI 1640 supplemented with 10% FCS and 100 ng/mL LPS plus 20 ng/mL IFN-gamma (M1 polarization) or 20 ng/mL IL-4 (M2 polarization) for 24 h. When needed, chemical inhibitors were added with IL-4.

2011-09-15 | E-GEOD-32164 | biostudies-arrayexpress

Effect of TAFA4 on Human macrophage M2c polarization

Project description:We aimed to decipher the effect of the neuropeptide TAFA4 on human M2c macrophage polarization. We used monocytes isolated from peripheral blood of three independant donors and generated different polarisations in the presence or absence of TAFA4. Monocytes were cultured with M-CSF for six days to induce their differentiation in macrophages (Mφ). On day six, the cells were left untreated or were treated for two days with dexamethasone to induce their M2c polarization. After differentiation and polarization, 100,000 cells from each condition and donor were sorted to remove debris and dead cells, then used for the sequencing.

2024-06-30 | GSE181185 | GEO

The effect of CNF1 on macrophage polarization

Project description:Research on the mechanism of Cytotoxic Necrotizing Factor 1 in regulating macrophage polarization.To study the molecular mechanisms through which CNF1 induces M1 macrophage polarization, we analyzed gene expression profiles of BMDMs treated with CNF1 or dialysis buffer.

2022-06-20 | GSE184193 | GEO

Modulation of macrophage polarization by HMB [macrophage]

Project description:Modulation of macrophage polarization by HMB [macrophage]

| PRJNA739181 | ENA

TIPE1 regulation on macrophage polarization

Project description:TIPE1 regulation on macrophage polarization

| PRJNA759608 | ENA

Branched-chain ketoacids derived from cancer cells modulate macrophage polarization and metabolic reprogramming

Project description:<p>Macrophages are prominent immune cells in the tumor microenvironment that can be educated into pro-tumoral phenotype by tumor cells to favor tumor growth and metastasis. The mechanisms that mediate a mutualistic relationship between tumor cells and macrophages remain poorly characterized. Here, we have shown <em>in vitro</em> that different human and murine cancer cell lines release branched‐chain α‐ketoacids (BCKAs) into the extracellular milieu, which influence macrophage polarization in an monocarboxylate transporter 1 (MCT1)‐dependent manner. We found that α‐ketoisocaproate (KIC) and α‐keto‐β‐methylvalerate (KMV) induced a pro‐tumoral macrophage state, whereas α‐ketoisovalerate (KIV) exerted a pro‐inflammatory effect on macrophages. This process was further investigated by a combined metabolomics/proteomics platform. KMV and KIC altered macrophage tricarboxylic acid (TCA) cycle intermediates and increased polyamine metabolism. Proteomic and pathway analyses revealed that the three BCKAs, especially KMV, exhibited divergent effects on the inflammatory signal pathways, phagocytosis, apoptosis and redox balance. These findings uncover cancer‐derived BCKAs as novel determinants for macrophage polarization with potential to be selectively exploited for optimizing antitumor immune responses.</p>

2022-10-03 | MTBLS4497 | MetaboLights

Frank2021 - Macrophage polarization

Project description:The model describes the mechanisms by which macrophages differentiate into a given phenotype. The model shows that both extracellular and intracellular signalling are both important for that process. More specifically, STAT1 activity favors macrophages polarization towards M1 phenotype and STAT6 activity favors macrophage polarization towards M2 phenotype. However, these polarizations are can be reversed by molecular signalling.

2024-09-02 | BIOMD0000001060 | BioModels

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