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Targeting low levels of MIF expression as a potential therapeutic strategy for ALS

ABSTRACT: Targeting low levels of MIF expression as a potential therapeutic strategy for ALS

PROVIDER: PRJNA1032865 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26544424_1.fastq.gz	Fastqsanger.gz
	SRR26544424_2.fastq.gz	Fastqsanger.gz
	SRR26544425_1.fastq.gz	Fastqsanger.gz
	SRR26544425_2.fastq.gz	Fastqsanger.gz
	SRR26544426_1.fastq.gz	Fastqsanger.gz

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Targeting low levels of MIF expression as a potential therapeutic strategy for ALS

Project description:Mutations in SOD1 cause amyotrophic lateral sclerosis (ALS), a neurodegenerative disease characterized by motor neurons (MNs) loss. We previously discovered that macrophage migration inhibitory factor (MIF), whose levels are extremely low in spinal MNs, inhibits mutant SOD1 misfolding and toxicity. In this study, we show that a single peripheral injection of adeno-associated virus (AAV) delivering MIF into adult SOD1G37R mice, significantly improved their motor function, delayed disease progression and extended survival. Moreover, MIF treatment reduced neuroinflammation and misfolded SOD1 accumulation, rescued MNs and corrected dysregulated pathways as observed by proteomics and transcriptomics. Furthermore, we revealed low MIF levels in human induced pluripotent stem cell derived MNs from familial ALS patients with different genetic mutations, as well as in post-mortem tissues of sporadic ALS patients. Our findings indicate that peripheral MIF administration may provide a potential therapeutic mechanism for modulating misfolded SOD1 in vivo and disease outcome in ALS patients.

2024-01-11 | GSE246397 | GEO

Targeting low levels of MIF expression as a potential therapeutic strategy for ALS

Project description:CSF was collected from non-transgenic and SOD1-G37R transgenic mice not treated or treated with AAV-PHP.eB-MIF using single tail-vein injection after the disease onset.

2024-05-03 | PXD046619 | Pride

microRNA Expression Profiling of MIF-high and MIF-low Pancreatic Ductal Adenocarcinoma using Nanostring nCounter Platform

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

microRNA Expression Profiling of MIF-high and MIF-low Pancreatic Ductal Adenocarcinoma using Nanostring nCounter Platform

2016-06-01 | GSE62498 | GEO

Transcription profiling of wounds from ovariectomized MIF null mice and controls to investigate the role of MIF during wound healing using BALB/C MIF null mice

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

A Global Genomic View of MIF Knockdown Cell

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.

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A Global Genomic View of MIF Knockdown Cell

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Gene regulation following MIF stimulation.

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.

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Project description:Amyotrophic lateral sclerosis (ALS) is a paralytic degenerative disease of the nervous system. In the SOD1 mouse model of ALS we found loss of the molecular and functional microglia signature associated with pronounced expression of miR-155 in SOD1 mice. We also found increased expression of miR-155 in the spinal cord of ALS subjects. Genetic ablation of miR-155 increased survival in SOD1 mice and reversed the abnormal microglial and monocyte molecular signature. In addition, dysregulated proteins in the spinal cord of SOD1 mice that we identified in human ALS spinal cords and CSF were restored in SOD1G93A/miR155-/- mice. Treatment of SOD1 mice with anti-miR-155 SOD1 mice injected systemically or into the cerebrospinal fluid prolonged survival and restored the microglial unique genetic and microRNA profiles. Our findings provide a new avenue for immune based therapy of ALS by targeting miR-155. Total RNA was isolated from whole lumbar spinal cord homogenate from healthy control donors without known neurologic diseases and sporadic and familial ALS.

2014-11-24 | E-GEOD-52946 | biostudies-arrayexpress

Transcriptome profiling of neutrophils in curdlan-injected Wild Type SKG mice and Mif KO (Mif -/-) SKG mice

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

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