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Loss of TET2 Impairs Endothelial Angiogenesis via Downregulating STAT3 Target Genes

ABSTRACT: Loss of TET2 Impairs Endothelial Angiogenesis via Downregulating STAT3 Target Genes

PROVIDER: PRJNA822838 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18590600_1.fastq.gz	Fastqsanger.gz
	SRR18590600_2.fastq.gz	Fastqsanger.gz
	SRR18590601_1.fastq.gz	Fastqsanger.gz
	SRR18590601_2.fastq.gz	Fastqsanger.gz
	SRR18590602_1.fastq.gz	Fastqsanger.gz

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Loss of TET2 Impairs Endothelial Angiogenesis via Downregulating STAT3 Target Genes

Project description:To investigate the role of TET2 in HUVECs under hypoxia, HUVECs were exposed to an atmosphere of 1% oxygen, 5% CO2 and 94% N2 for 48 h, in which TET2 had been knocked down by siRNA. We then performed gene expression profiling analysis using data obtained from RNA-seq of HUVECs transfected with control siRNA or TET2 siRNA.

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Loss of TET2 impairs endothelial angiogenesis via downregulating STAT3 target genes.

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Project description:Angiogenesis is a tightly regulated process essential for both development and disease, yet the role of fibroblast growth factor 13 (FGF13) in vascular remodeling has remained unclear. Here, we identify FGF13 as a key negative regulator of physiological and pathological angiogenesis. Using endothelial cell–specific knockout and overexpression mouse models, combined with retinal vascularization assays, hindlimb ischemia and myocardial infarction models, and in vitro endothelial cell functional assays, we demonstrate that loss of FGF13 enhances, whereas its overexpression impairs, neovascularization. Mechanistically, FGF13 binds to the PAS domain of HIF-1α and facilitates its interaction with RACK1, leading to oxygen-independent degradation of HIF-1α and suppression of downstream angiogenic signaling. Importantly, adenoviral overexpression of HIF-1α reversed the inhibitory effects of FGF13, confirming its essential role in mediating FGF13-driven angiogenic regulation. These findings reveal FGF13 as a critical endothelial-intrinsic brake on angiogenesis and suggest its potential as a therapeutic target in ischemic vascular disease.

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