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Transcriptomic data of whole liver from Alk1-(alias Acvrl1) knockout mice I

ABSTRACT: Transcriptomic data of whole liver from Alk1-(alias Acvrl1) knockout mice I

PROVIDER: PRJNA766053 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16048287.fastq.gz	Fastqsanger.gz
	SRR16048288.fastq.gz	Fastqsanger.gz
	SRR16048289.fastq.gz	Fastqsanger.gz
	SRR16048290.fastq.gz	Fastqsanger.gz
	SRR16048291.fastq.gz	Fastqsanger.gz

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Transcriptomic data of whole liver from Alk1-(alias Acvrl1) knockout mice I

Project description:Hereditary hemorrhagic telangiectasia (HHT, alias Rendu-Osler-Weber syndrome) is an autosomal dominant genetic disease that causes vascular malformations in multiple organs. Malformations and shunts in the liver are relevant for the long-term prognosis as they can lead to heart failure. Moreover, the role of ALK-1 in the hepatic vascular niche remains elusive. In this project, we aimed to establish a novel HHT model covering hepatic involvement by the disease and to investigate the role of ALK-1 in the hepatic vascular niche. We crossed Stab2-icre mice (MGI: 6741034) with Acvrl1-floxed mice (MGI: 4398901) to generate constitutive hepatic endothelial Acvrl1 knockout (Acvrl1-HEC-KO, alias Alk1-HEC-KO) mice. To dissect hepatic transcriptomic alterations, we performed RNA sequencing of freshly isolated whole liver cells from 3 months old mice. Transcriptomic analyses revealed an arterialization of hepatic vessels accompanied by loss of LYVE-1 and induction of Endomucin. The loss of endothelial Wnt2, Wnt9b, and Rspo3 led to a disruption of hepatic metabolic zonation with a dominance of periportal genes in Alk1-HEC-KO mice and HHT patients. Furthermore, we identified PRND (alias Doppel) and placenta growth factor (PlGF) as novel candidates of HHT pathogenesis in mice. ALK-1 controls hepatic metabolic zonation via Wnt signaling and suppresses PRND and PlGF that represent novel candidates in HHT pathogenesis.

2023-04-06 | GSE184746 | GEO

Transcriptomic data of liver endothelial cells from Alk1-(alias Acvrl1) knockout mice II

Project description:Hereditary hemorrhagic telangiectasia (HHT, alias Rendu-Osler-Weber syndrome) is an autosomal dominant genetic disease that causes vascular malformations in multiple organs. Malformations and shunts in the liver are relevant for the long-term prognosis as they can lead to heart failure. Moreover, the role of ALK-1 in the hepatic vascular niche remains elusive. In this project, we aimed to establish a novel HHT model covering hepatic involvement by the disease and to investigate the role of ALK-1 in the hepatic vascular niche. We crossed Stab2-icre mice (MGI: 6741034) with Acvrl1-floxed mice (MGI: 4398901) to generate constitutive hepatic endothelial Acvrl1 knockout (Acvrl1-HEC-KO, alias Alk1-HEC-KO) mice. To dissect microvascular transcriptomic alterations, we performed RNA sequencing of freshly isolated hepatic endothelial cells from 3 months old mice. Transcriptomic analyses revealed an arterialization of hepatic vessels accompanied by loss of LYVE-1 and induction of Endomucin. The loss of endothelial Wnt2, Wnt9b, and Rspo3 led to a disruption of hepatic metabolic zonation with a dominance of periportal genes in Alk1-HEC-KO mice and HHT patients. Furthermore, we identified PRND (alias Doppel) and placenta growth factor (PlGF) as novel candidates of HHT pathogenesis in mice. ALK-1 controls hepatic metabolic zonation via Wnt signaling and suppresses PRND and PlGF that represent novel candidates in HHT pathogenesis.

2023-04-06 | GSE184747 | GEO

Transcriptomic data of liver endothelial cells from Alk1-(alias Acvrl1) knockout mice

Project description:Transcriptomic data of liver endothelial cells from Alk1-(alias Acvrl1) knockout mice

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Transcriptomic data of liver endothelial cells from Alk1-(alias Acvrl1) knockout mice II

Project description:Transcriptomic data of liver endothelial cells from Alk1-(alias Acvrl1) knockout mice II

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ALK1/Smad4 signaling is required for the identity of Kupffer cells and prevention of bacterial infection.

Project description:RNA Sequencing of liver Kupffer cells and and monocyte-derived macrophages (MoMs) to assess role of ALK1 and Smad4.

2024-06-30 | GSE151870 | GEO

Transcriptomic data from the liver of Ahr knockout mice

Project description:Transcriptomic data from the liver of Ahr knockout mice