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Single-cell Transcriptome Analysis Reveals the Dynamic Populations of Vascular Cells in Neointimal Hyperplasia

ABSTRACT: Single-cell Transcriptome Analysis Reveals the Dynamic Populations of Vascular Cells in Neointimal Hyperplasia

PROVIDER: PRJNA1021991 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26204592.fastq.gz	Fastqsanger.gz
	SRR26204592_1.fastq.gz	Fastqsanger.gz
	SRR26204592_2.fastq.gz	Fastqsanger.gz
	SRR26204593_1.fastq.gz	Fastqsanger.gz
	SRR26204593_2.fastq.gz	Fastqsanger.gz

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Single-cell Transcriptome Analysis Reveals the Dynamic Populations of Vascular Cells in Neointimal Hyperplasia

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Inhibition of PARP 1 Protects Against Hyperglycemic-induced Neointimal Hyperplasia by Upregulating TFPI-2 Activity

Project description:To investigate the function and potential mechanism of PARP-1 poly(ADP-ribose) polymerase 1 (PARP1) in diabetic neointimal hyperplasia. Type 1 diabetes mellitus was induced using streptozotocin (STZ) in wild-type mice and PARP1-/- mice, and ligation of the left carotid artery was performed to induce neointimal hyperplasia. Ligated carotid arteries from diabetic mice developed more extensive neointimal hyperplasia and showed greater proliferation and migration than arteries from nondiabetic mice. The augmented remodeling response was absent in diabetic mice deficient in PARP1. PARP1 deficiency reduces diabetic neointimal hyperplasia by upregulating tissue factor pathway inhibitor (TFPI)-2, which acted as a suppressor of vascular smooth muscle cell (VSMCs) proliferation and migration. The underlying mechanisms involve PARP1 that acts as a negative transcription factor by enhancing TFPI-2 promoter DNA methylation. Our studies demonstrated for the first time that Inhibition of PARP1 alleviates neointimal hyperplasia in diabetes by up-regulating TFPI-2 expression and blocking VSMC proliferation and migration. The development of PARP1 inhibitors might serve to limit mainly proliferative and migratory processes in restenosis-prone diabetic patients

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