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TWEAK/Fn14 axis is a therapeutic target for post-angioplasty restenosis

ABSTRACT: TWEAK/Fn14 axis is a therapeutic target for post-angioplasty restenosis

PROVIDER: PRJNA465344 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7132180_1.fastq.gz	Fastqsanger.gz
	SRR7132180_2.fastq.gz	Fastqsanger.gz
	SRR7132181_1.fastq.gz	Fastqsanger.gz
	SRR7132181_2.fastq.gz	Fastqsanger.gz
	SRR7132176_1.fastq.gz	Fastqsanger.gz

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TWEAK/Fn14 axis is a therapeutic target for post-angioplasty restenosis

Project description:Aim: Next generation sequencing-based methods were performed to identify genes and pathways regulated by TWEAK in VSMCs Methods: Using a gene-set enrichment method, we found a functional module involved in cell proliferation defined as the minimal network connecting top TWEAK up-regulated genes. Results: TWEAK increased the number of VSMCs in S phase and the total number of proliferative cells. Conclusions: Our data define a major role of TWEAK/Fn14 in the control of VSMCs proliferation and migration during neointimal hyperplasia after wire injury in mice, and identify TWEAK/Fn14 as a potential target for treating restenosis after angioplasty. provide a framework for comparative investigations of expression profiles. Our results show that NGS offers a comprehensive and more accurate quantitative and qualitative evaluation of mRNA content within a cell or tissue. We conclude that RNA-seq based transcriptome characterization would expedite genetic network analyses and permit the dissection of complex biologic functions.

2020-03-03 | GSE114166 | GEO

TMT-coupled phosphoproteomics support novel role of TWEAK/Fn14 signaling in synaptic function

Project description:The study aims at illustrate novel role of TWEAK/Fn14 signaling in synapse function by combining electrophysiological and phosphoproteomic approaches. The results show that TWEAK acutely dampens basal synaptic transmission and plasticity through neuronal Fn14 and impacts the phosphorylation state of pre- and post-synaptic proteins in adult mouse hippocampal slices. Two models featuring synaptic deficits were used in the study. Blocking TWEAK/Fn14 signaling augments synaptic function in hippocampal slices from amyloid beta-overexpressing mice. After stroke, genetic or pharmacological inhibition of TWEAK/Fn14 signaling augments basal synaptic transmission and normalizes plasticity. Our data support a glial/neuronal axis that critically modifies synaptic physiology and pathophysiology in different contexts in the mature brain and may be a therapeutic target for improving neurophysiological outcomes.

2021-02-02 | PXD021582 | Pride

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