Modulation of macrophage polarization by HMB [tumor]
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ABSTRACT:
PROVIDER: PRJNA739183 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Modulation of macrophage polarization by HMB [macrophage]
| PRJNA739181 | ENA
Project description:Modulation of macrophage polarization by HMB
| PRJNA739180 | ENA
Project description:Modulation of macrophage polarization by HMB [muscle]
| PRJNA739182 | ENA
Project description:to determine whether hydroxymethyl butyrate alters macrophage polarization bone marrow derived macrophages were treated with HMB alone or in combination with LPS for 48h
2021-12-29 | GSE178475 | GEO
Project description:to determine whether hydroxymethyl butyrate alters PDAC response to anti-PD1 therapy, mice bearing PANC02 tumors were treated with anti-PD1 with or without HMB supplementation
2021-12-29 | GSE178477 | GEO
Project description:to determine whether hydroxymethyl butyrate alters PDAC response to anti-PD1 therapy, mice bearing PANC02 tumors were treated with anti-PD1 with or without HMB supplementation, gastroc mucsle was isolated from ctrl and HMB groups and analysed by microarray for HMB induced differences in gene expression
2021-12-29 | GSE178476 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2021-12-29 | GSE178478 | GEO
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
Project description:Macrophages are innate immune cells characterized by their plasticity and their ability to react to various environmental stimuli. These cells are involved in a multiple number of tissular functions in homeostasis and pathological contexts. According to their environment these cells could be polarized toward different states of activation which determine their functional orientation. A large part of the macrophage biology field is devoted to better define what polarizations are, from a molecular point of view. It is now accepted that a multidimensional model of polarization is needed to grasp the broad phenotype repertoire depending on various environmental signals. Oxygen tension is one of these tissular environmental parameters. We designed this study to obtain a proteomic signature of various polarizations in human monocytes derived macrophages. We also seek to explore how environmental oxygen tension varying from an atmospheric composition (18.6% O2) to a “tissular normoxia” (3% O2) could modify our classification of macrophages’ polarization. We have obtained various polarization specific proteins and oxygen sensors for human macrophages. One example is arachidonate 15-lipoxygenase (ALOX15) which is a IL4/IL13 polarization specific proteins up regulated under low oxygen exposure associated to an increase of the phagocytosis rate of apoptotic cells. These results illustrate the necessity to take into account physicochemical parameters like oxygen when macrophage polarization is studied to correctly assess their functions in tissues.
2017-09-11 | PXD006354 | Pride
Project description:This model is based on:
Computational Modeling of the Crosstalk Between Macrophage Polarization and Tumor Cell Plasticity in the Tumor Microenvironment.
Abstract:
Tumor microenvironments contain multiple cell types interacting among one another via different signaling pathways. Furthermore, both cancer cells and different immune cells can display phenotypic plasticity in response to these communicating signals, thereby leading to complex spatiotemporal patterns that can impact therapeutic response. Here, we investigate the crosstalk between cancer cells and macrophages in a tumor microenvironment through in silico (computational) co-culture models. In particular, we investigate how macrophages of different polarization (M1 vs. M2) can interact with epithelial-mesenchymal plasticity of cancer cells, and conversely, how cancer cells exhibiting different phenotypes (epithelial vs. mesenchymal) can influence the polarization of macrophages. Based on interactions documented in the literature, an interaction network of cancer cells and macrophages is constructed. The steady states of the network are then analyzed. Various interactions were removed or added into the constructed-network to test the functions of those interactions. Also, parameters in the mathematical models were varied to explore their effects on the steady states of the network. In general, the interactions between cancer cells and macrophages can give rise to multiple stable steady-states for a given set of parameters and each steady state is stable against perturbations. Importantly, we show that the system can often reach one type of stable steady states where cancer cells go extinct. Our results may help inform efficient therapeutic strategies.
2019-09-23 | MODEL1909230002 | BioModels