MIF promotes cell invasion by LRP1-uPAR interaction in pancreatic cancer cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE212201 | GEO | 2022/12/31
REPOSITORIES: GEO
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Project description:MIF promotes cell invasion by LRP1-uPAR interaction in pancreatic cancer cells
| PRJNA874449 | ENA
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:siRNA-mediated knockdown of MIF expression in HEK293 cells resulted in inhibition of cell proliferation and cell cycle progress. The microarray study of MIF KD cells reveald knockdown of MIF would lead to extensive changes in gene expression profiles which may elucidate the molecular mechanism of MIF siRNA-mediated inhibition of cell cycle and cell proliferation. Keywords: The whole-genome expression analysis in MIF knockdown cells and the control cells HEK293 cells were transfected MIF siRNA (50pmol/ml & 100pmol/ml) or control RNA using LipofectamineTM 2000 reagent and re-incubated for 24 hours.At the designed time point, totol RNA was isolated from the different treated cells.The normal cells were used as control.
2009-11-02 | E-GEOD-10241 | biostudies-arrayexpress
Project description:We identified differentially expressed microRNAs between MIF-high and MIF-low tumor groups. These microRNAs were then investigated for their potential downstream targets using an integrative strategy, which combines miR-Walk target prediction module and mRNA expression array data to identify key MIF-induced signalling pathways driving tumor progresion and disease aggressiveness. Genes that associated with prognostic significance was then subjected to mechanistic study. miRNA expression profiling of 69 pancreatic ductual adenocarcinoma was performed in two sets. The batch effect between the two sets of data was removed using Partek Genomic Suite
2016-06-01 | E-GEOD-62498 | biostudies-arrayexpress
Project description:siRNA-mediated knockdown of MIF expression in HEK293 cells resulted in inhibition of cell proliferation and cell cycle progress. The microarray study of MIF KD cells reveald knockdown of MIF would lead to extensive changes in gene expression profiles which may elucidate the molecular mechanism of MIF siRNA-mediated inhibition of cell cycle and cell proliferation. Keywords: The whole-genome expression analysis in MIF knockdown cells and the control cells
2009-11-03 | GSE10241 | GEO
Project description:We identified differentially expressed microRNAs between MIF-high and MIF-low tumor groups. These microRNAs were then investigated for their potential downstream targets using an integrative strategy, which combines miR-Walk target prediction module and mRNA expression array data to identify key MIF-induced signalling pathways driving tumor progresion and disease aggressiveness. Genes that associated with prognostic significance was then subjected to mechanistic study.
2016-06-01 | GSE62498 | GEO
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:Lasting B-cell persistence depends on survival signals that are transduced by cell surface receptors. Here, we describe a novel biological mechanism essential for survival and homeostasis of normal peripheral mature B cells and chronic lymphocytic leukemia (CLL) cells, regulated by the heparin-binding cytokine, midkine (MK), and its proteoglycan receptor, the receptor-type tyrosine phosphatase zeta (RPTPζ). We demonstrate that MK initiates a signaling cascade leading to B cell survival, by binding to RPTPζ. In mice lacking PTPRZ, the proportion and number of the mature B cell population is reduced. Our results emphasize a unique and critical function for MK signaling in the previously described MIF/CD74 induced survival pathway. Stimulation of CD74 with MIF leads to c-Met activation, resulting in elevation of MK expression in both normal mouse splenic B and CLL cells. Our results indicate that MK and RPTPζ are important regulators of the B cell repertoire. These findings could pave the way towards understanding the mechanisms shaping B cell survival, and suggest novel therapeutic strategies based on the blockade of the midkine/RPTPζ-dependent survival pathway. 2 samples were incubated with or without MIF.
2011-11-01 | E-GEOD-33352 | biostudies-arrayexpress
Project description:The curdlan-injected SKG mouse is a mouse model of spondyloarthritis. We identified neutrophils are one of the major immune cells produing MIF in the SKG mice. In this study, we performed total RNA sequecing analysis to identify differentially expressed protein-coding genes (DEGs) in neutrophils isolated from wild type SKG mice comapred to neutrophils isolated from Mif -/- SKG mice after curdlan treatment.
2021-07-31 | GSE180997 | GEO
Project description:Atherosclerosis is a chronic inflammatory condition of our arteries and the main underlying pathology of myocardial infarction and stroke. The pathogenesis is age-dependent, but the links between disease progression, age, and atherogenic cytokines and chemokines are incompletely understood. Here, we studied the chemokine-like inflammatory cytokine macrophage migration inhibitory factor (MIF) in atherogenic Apoe–/– mice across different stages of aging and cholesterol-rich high-fat diet (HFD). MIF promotes atherosclerosis by mediating leukocyte recruitment, lesional inflammation, and suppressing atheroprotective B- cells. However, links between MIF and advanced atherosclerosis across aging have not been systematically explored. We compared effects of global Mif-gene deficiency in 30-, 42-, and 48-week-old Apoe–/– mice on HFD for 24, 36, or 42 weeks, respectively, and in 52-week- old mice on a 6-week HFD. Mif-deficient mice exhibited reduced atherosclerotic lesions in the 30/24- and 42/36-week-old groups, but atheroprotection, which in the applied Apoe–/– model was limited to lesions in the brachiocephalic artery and abdominal aorta, was not detected in the 48/42- and 52/6-week-old groups. This suggested that atheroprotection afforded by global Mif-gene deletion differs across aging stages and atherogenic diet duration. To characterize this phenotype and study the underlying mechanisms, we determined immune cells in the periphery and vascular lesions, obtained a multiplex cytokine/chemokine profile, and compared the transcriptome between the age-related phenotypes. We found that Mif- deficiency promotes lesional macrophage and T cell counts in younger but not aged mice, with sub-group analysis pointing towards a role for Trem2+ macrophage. The transcriptomic analysis identified MIF- and aging-dependent changes in lipid, cell respiration, and inflammation pathways, and key enriched genes such as Cpne7, Cd6, Plin1, Cd274 hinting towards effects on lesional T cells, lipids, and foamy macrophages. Moreover, Mif-deficient aged mice exhibited a distinct plasma cytokine/chemokine signature consistent with the notion that mediators known to drive inflamm’aging are either not down-regulated or even up- regulated in Mif-deficient aged mice compared to the corresponding younger ones. Lastly, Mif-deficiency favored formation of lymphocyte-rich peri-adventitial leukocyte clusters. While the causative contributions of these mechanistic pillars and their interplay will be subject to future scrutiny, our study suggests that atheroprotection due to global Mif-gene deficiency in atherogenic Apoe–/– mice is reduced upon advanced aging and identifies previously unrecognized cellular and molecular targets that could explain this phenotype shift. These observations enhance our understanding of inflamm’aging and MIF pathways in atherosclerosis and may have implications for translational MIF-directed strategies.
2022-12-21 | GSE221504 | GEO