Role of Macrophage migration inhibitory factor (MIF) in pancreatic stellate cells (PSCs)
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ABSTRACT:
PROVIDER: PRJEB39522 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR4368610_1.fastq.gz | Fastqsanger.gz | |||
| ERR4368610_2.fastq.gz | Fastqsanger.gz | |||
| ERR4368611_1.fastq.gz | Fastqsanger.gz | |||
| ERR4368611_2.fastq.gz | Fastqsanger.gz | |||
| ERR4368612_1.fastq.gz | Fastqsanger.gz |
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Project description:The presence of activated pancreatic stellate cells (PSCs) in the pancreatic ductal adenocarcinoma (PDAC) microenvironment plays a significant role in cancer progression. Macrophage migration inhibitory factor (MIF) is overexpressed in PDAC tissues and expressed by both cancer and stromal cells. The expression status of MIF and its receptors in PDAC- associated fibroblasts or PSCs and its pathophysiological roles are yet to be elucidated. The next-generation sequencing technique was adapted to check the effect of MIF absence on the expression of other genes in mice (mPSCs).
2022-09-28 | E-MTAB-9392 | biostudies-arrayexpress
Project description:NIH 3T3 fibroblasts that express little detectable levels of the MIF binding receptor CD74 but do express the signalling component CD44 were used for the identification of interacting proteins that are shared by MIF and D-DT. Endogenously expressed MIF and D-DT were tagged at the C-terminus using a short sequence that is recognized and biotinylated by the bacterial biotin ligase BirA (Efficient biotinylation and single-step purification of tagged transcription factors in mammalian cells and transgenic mice. Proc. Natl. Acad. Sci. U. S. A. 100, 7480–5) as described in detail for MIF Filip, A. M. et al. (2009). Ribosomal Protein S19 Interacts with Macrophage Migration Inhibitory Factor and Attenuates Its Pro-inflammatory Function. J. Biol. Chem. 284, 7977–7985). After pulling down biotinylated proteins from stable NIH 3T3 clones that express tagged MIF or D-DT and BirA ligase with streptavidin agarose, bound proteins were separated by SDS-PAGE and identified after elution and tryptic digestion by mass spectrometry in order to characterize the MIF and D-DT interactomes.
2021-01-27 | PXD020449 | Pride
Project description:Role of Macrophage migration inhibitory factor (MIF) in pancreatic stellate cells (PSCs)
2023-06-16 | E-MTAB-9392 | ExpressionAtlas
Project description:The aim of this experiment was to investigate the role of MIF during wound healing using BALB/C MIF null mice and in the context of reduced estrogen-associated impaired healing using ovariectomized mice (a mouse model of age-associated delayed healing). Ageing is associated with delayed cutaneous wound healing resulting from reduced estrogen levels. Macrophage migration inhibitory factor (MIF - NCBI RefSeq: NM_010798) is thought to mediate the effects of estrogen on wound healing. Gene expression was compared between wounds from ovariectomized MIF null mice and controls.
2005-11-05 | E-MEXP-209 | biostudies-arrayexpress
Project description:Background: Hepatic ischemia–reperfusion (I/R) injury is a major complication leading to surgical failures in liver resection, transplantation, and hemorrhagic shock. The role of cytokine macrophage migration inhibitory factor (MIF) in hepatic I/R injury is unclear. Methods: We examined changes of MIF expression in mice after hepatic I/R surgery and hepatocytes challenged with hypoxia–reoxygenation (H/R) insult. Subsequently, MIF global knock-out mice and mice with adeno-associated-virus (AAV)-delivered MIF overexpression were subjected to hepatic I/R injury. Hepatic histology, the inflammatory response, apoptosis and oxidative stress were monitored to assess liver damage. The molecular mechanisms of MIF function were explored in vivo and in vitro. Results: MIF was significantly upregulated in the serum whereas decreased in liver tissues of mice after hepatic I/R injury. MIF knock-out effectively attenuated I/R -induced liver inflammation, apoptosis and oxidative stress in vivo and in vitro, whereas MIF overexpression significantly aggravated liver injury. Via RNA-seq analysis, we found a significant decreased trend of MAPK pathway in MIF knock-out mice subjected hepatic I/R surgery. Using the apoptosis signal-regulating kinase 1 (ASK1) inhibitor NQDI-1 we determined that, mechanistically, the protective effect of MIF deficiency on hepatic I/R injury was dependent on the suppressing of the ASK1-JNK/P38 signaling pathway. Moreover, we found MIF inhibitor ISO-1 alleviate hepatic I/R injury in mice. Conclusion: Our results confirm that MIF deficiency suppresses the ASK1-JNK/P38 pathway and protects the liver from I/R -induced injury. Our findings suggest MIF as a novel biomarker and therapeutic target for the diagnosis and treatment of hepatic I/R injury.. We then performed gene expression profiling analysis using data obtained from RNA-seq of 6 different liver tissues of mice subjected to hepatic I/R injury.
2022-09-28 | GSE212508 | GEO
Project description:Firstly, the adductome of he protein macrophage migration inhibitory factor (MIF) with different haptens encompassing different reaction mechanisms and potencies was investigated. After incubation of MIF with the different haptens at 5 times molar excess of hapten, an untargeted Full MS/dd-MS2 experimental approach was used with a QExactive Quadrupole-Orbitrap mass spectrometer. The data were processed with Proteome Discoverer and the suggested sites of adductions were confirmed in parallel reaction monitoring mode (PRM) on the same instruments.
2022-03-18 | PXD031793 | Pride
Project description:Firstly, the adductome of the two major mouse blood proteins, as well as of the protein macrophage migration inhibitory factor (MIF) with the model hapten tetramethylrhodamine isothiocyanate (TRITC)was invastigated. After incubation at different molar ratios of TRITC, an untargeted Full MS/dd-MS2 experimental approach was used with a QExactive Quadrupole-Orbitrap mass spectrometer. The data were processed with Proteome Discoverer and the suggested sites of adductions were confirmed in parallel reaction monitoring mode (PRM) on the same instruments. Blood and lymph node samples of mise treated topically with the same hapten were screened for the peptides containing the most reactive sites of the aformentioned proteins. Only the adducted N-terminal peptide of the protein MIF could be detected. Thereafter, a quantification approach in PRM mode using standards was implemented to quantify this peptide, both modified and unmodified. Quantification was based in characteristic b and y ions.
2022-04-08 | PXD031143 | Pride
Project description:Despite the demonstrated efficacy of immune checkpoint blockade therapies in various tumors, their efficacy in cervical cancer is limited by factors such as the need for positive PD-L1 expression and the development of drug resistance. A crucial pro-inflammatory cytokine, macrophage migration inhibitory factor (MIF), is highly expressed in various cancers and contributes to tumor progression by regulating inflammatory responses and the tumor microenvironment. The present study aimed to explore the role of macrophage migration inhibitory factors in cervical squamous cell carcinoma (CSCC) recurrence and metastasis. Western blotting, reverse transcription quantitative PCR, cell-counting kit 8 assay, flow cytometry, and ELISA were used to investigate the effects of MIF on CSCC progression and formation of inflammasomes. Transcriptome and proteome sequencing were combined to screen for key effector proteins of MIF. Moreover, in vitro co-culture experiments, Transwell assays, and flow cytometry were used to evaluate the roles of MIF and TSC22 domain family protein 3 (TSC22D3) as inflammatory tumor-promoting factors in macrophage recruitment and polarization induction. The results indicated that MIF was highly expressed in CSCC with lymph node metastasis, positively correlated with cervical cancer stage, and associated with poor prognosis. MIF was found to promote CSCC progression and linked to inflammasome activation. Multi-omics screening results indicated that TSC22D3 may be a crucial interacting gene of MIC. Moreover, MIF and TSC22D3 could facilitate inflammasome activation, macrophage recruitment, and M2 polarization. Therefore, MIF and TSC22D3 can induce macrophage infiltration in cervical cancer lesions and affect the tumor microenvironment by polarizing macrophages toward the M2 phenotype, promoting CSCC progression. This study highlights the potential of targeting the MIF-TSC22D3 axis as a novel therapeutic strategy and offering a promising avenue for improving the efficacy of immunotherapy in treatin
2025-01-26 | PXD057462 | Pride
Project description:Somatic mutation in TET2 gene is one of the most common clonal genetic events detected in age-related clonal hematopoiesis as well as in chronic myelomonocytic leukemia (CMML). In addition to being a pre-malignant state, TET2 mutated clones are associated with an increased risk of death from cardiovascular disease, which could involve cytokine/chemokine overproduction by monocytic cells. Here, we show in mice and in human cells that, in the absence of any inflammatory challenge, TET2 down-regulation promotes the production of MIF (macrophage migration inhibitory factor), a pivotal mediator of atherosclerotic lesion formation. In healthy monocytes, TET2 is recruited to MIF promoter and interacts with the transcription factor EGR1 and histone deacetylases. Disruption of these interactions as a consequence of TET2-decreased expression favors EGR1-driven transcription of MIF gene and its secretion. MIF favors monocytic differentiation of myeloid progenitors. These results designate MIF as a chronically overproduced chemokine and a potential therapeutic target in patients with clonal TET2 down-regulation in myeloid cells.
2021-11-13 | GSE188624 | GEO
Project description:Macrophage migration inhibitory factor (MIF) is essential for Type 2 effector cell immunity to an intestinal helminth parasite
| PRJNA578060 | ENA