Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Identifying lncRNA-MM2P as a novel modulator of macrophage M2 polarization

ABSTRACT: Identifying lncRNA-MM2P as a novel modulator of macrophage M2 polarization

PROVIDER: PRJNA421988 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Identifying lncRNA-MM2P as a novel modulator of macrophage M2 polarization

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.

2018-11-20 | GSE107952 | GEO

Identifying lncRNAs as novel modulators of macrophage M2 polarization

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.

2018-11-20 | GSE107979 | GEO

Identifying lncRNAs as novel modulators of macrophage M2 polarization

Project description:Identifying lncRNAs as novel modulators of macrophage M2 polarization

| PRJNA422098 | ENA

TIPE regulates TGFB2 expression and induces extracellular M2 polarization in CRC

Project description:Abstract Background: M2 macrophages (M2) play a crucial role in the development of colorectal cancer (CRC). The elevated expression of TIPE in CRC is closely associated with CRC progression; however, the impact of TIPE on M2 polarization remains unclear. Methods: IHC, WB, flow cytometry, qPCR, and IF were used to verify the promoting effect of TIPE on M2 polarization in specimens and in vitro co-culture models. RNA-seq, ELISA, and WB were used to identify the secreted proteins regulated by TIPE and the underlying mechanism. CCK-8 assay, wound healing assay, and transwell invasion assay were used to verify the effect of M2 on CRC. In vivo experiments were used to identify the promoting effect of TIPE on M2 polarization. Results: In this study, we first demonstrated that the abnormal overexpression of TIPE in CRC promotes M2 polarization and is correlated with a poor prognosis for CRC patients. We then found that TIPE activates the P38 MAPK signaling pathway in CRC to regulate TGFΒ2 secretion and, furthermore, induces M2 macrophage polarization. In subcutaneous and lung xenograft models of CRC in nude mice, we found that TIPE regulates TGFΒ2 secretion from human CRC to promote M2 polarization of murine macrophages. Conclusion: These results indicate that TIPE is a potent oncogene for inducing M2 polarization. It is suggested that all cancers with high TIPE expression need to be alert to the production and infiltration of M2 macrophages, which provides a new perspective for cancer treatment.

2025-05-05 | GSE262823 | GEO

Identification of circular RNAs and mRNAs expression profiles in microglia M2 polarization [mRNA]

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.

2022-03-28 | GSE199399 | GEO

Identification of circular RNAs and mRNAs expression profiles in microglia M2 polarization [CircRNA]

2022-03-28 | GSE199398 | GEO

Targeting parvalbumin promotes M2 macrophage polarization energy expenditure in diet-induced mouse obesity models

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.

2022-05-10 | PXD033582 | Pride

Q11, a CYP2E1 inhibitor, exerts anti-hepatocellular carcinoma effect by inhibiting M2 macrophage polarization

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.

2024-12-26 | GSE282907 | GEO

Targeting BRD4 Ameliorates Experimental Emphysema Via Suppressing both M1 and M2 alveolar macrophage polarization-1

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

2024-01-09 | GSE250232 | GEO

The JMJD3-IRF4 axis regulates M2 macrophage polarization and host responses against helminth infection

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.

2010-08-22 | GSE23306 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data