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GMP after hindlimb ischemia

ABSTRACT: GMP after hindlimb ischemia

PROVIDER: PRJNA746955 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15150340.fastq.gz	Fastqsanger.gz
	SRR15150341.fastq.gz	Fastqsanger.gz
	SRR15150342.fastq.gz	Fastqsanger.gz
	SRR15150343.fastq.gz	Fastqsanger.gz
	SRR15150344.fastq.gz	Fastqsanger.gz

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GMP after hindlimb ischemia

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Project description:Peripheral Artery Disease is caused by the restriction or occlusion of arteries supplying the leg. Better understanding of the molecular mechanisms underpinning tissue response to acute and chronic ischemia is urgently needed to improve therapeutic options. The aim of this study is understanding miR-210 regulation and role in a mouse model of hindlimb ischemia. To investigate miR-210 function, mice were injected with a miR-210 complementary LNA-oligonucleotide (anti-miR-210). Then, the left femoral artery was dissected in order to induce unilateral hindlimb ischemia. Mice were sacrified 3 days later and gene expression profiles of gastrocnemius muscles were obatained.

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Transcriptome analysis of CD45-CD31+ endothelial cells in ischemic hindlimb muscle after IL-35 injection

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GPR174 Knockdown Enhances Blood Flow Recovery in Hindlimb Ischemia Mice Model by Upregulating AREG Expression

Project description:Regulatory T cells (Tregs) are critically involved in neovascularization, an important compensatory mechanism in peripheral artery disease (PAD). The contribution of G protein coupled receptor 174 (GPR174), which is a regulator of Treg function and development, in neovascularization remains elusive. Here, we reveal that genetic deletion of GPR174 in Tregs potentiated blood flow recovery in mice after hindlimb ischemia (HLI). GPR174 deficiency upregulates amphiregulin (AREG) expression in Tregs, thereby enhancing endothelial cell functions and reducing pro-inflammatory macrophage polarization and endothelial cell apoptosis. Mechanically, GPR174 regulates AREG expression by inhibiting the nuclear accumulation of early growth response protein 1 (EGR1) via Gαs/cAMP/PKA signal pathway activation. Collectively, these findings demonstrate that GPR174 negatively regulates angiogenesis and vascular remodeling in response to ischemic injury and that GPR174 may be a potential molecular target for therapeutic interventions of ischemic vascular diseases.

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