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E2F1 mediates SOX17 Deficiency-Induced Pulmonary Hypertension

ABSTRACT: E2F1 mediates SOX17 Deficiency-Induced Pulmonary Hypertension

PROVIDER: PRJNA792563 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17334856_1.fastq.gz	Fastqsanger.gz
	SRR17334856_2.fastq.gz	Fastqsanger.gz
	SRR17334857_1.fastq.gz	Fastqsanger.gz
	SRR17334857_2.fastq.gz	Fastqsanger.gz

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E2F1 mediates SOX17 Deficiency-Induced Pulmonary Hypertension

Project description:SRY-Box Transcription Factor 17 (SOX17) enhancers variants and mutations are found in patients with pulmonary arterial hypertension (PAH). In human PAH pulmonary microvascular endothelial cells (HPMVEC), there is a significant downregulation of SOX17 expression. We hypothesized that SOX17 deficiency contributes to the pathogenesis of PAH and found that mice with endothelial specific disruption (ecKO Sox17) developed spontaneous pulmonary hypertension (PH) and exacerbated hypoxia-induced PH. Loss of SOX17 in lung ECs induces cell cycle programming, proliferative and anti-apoptotic phenotypes, a process mediated by the activation of E2F Transcription Factor 1 (E2F1) signaling. Pharmacological inhibition of E2F1 in ecKO Sox17 mice attenuated PH and cell cycle programming. Our study demonstrated that endothelial SOX17 deficiency induces PH and targeting E2F1 signaling represents a promising approach in PAH patients.

2023-03-15 | GSE192649 | GEO

E2F1 mediates SOX17 Deficiency-Induced Pulmonary Hypertension [scRNA-seq]

Project description:SRY-Box Transcription Factor 17 (SOX17) enhancers variants and mutations are found in patients with pulmonary arterial hypertension (PAH). In human PAH pulmonary endothelial cells, there is a significant downregulation of SOX17 expression. We hypothesized that SOX17 deficiency contributes to the pathogenesis of PAH and found that mice with endothelial specific disruption (ecKO Sox17) developed spontaneous pulmonary hypertension (PH) and exacerbated hypoxia-induced PH. Loss of SOX17 in lung ECs induced endothelial dysfunctions including upregulation of cell cycle programming and paracrine effect, proliferative and anti-apoptotic phenotypes, impaired cellular junction and BMP signaling. E2F Transcription Factor 1 (E2F1) signaling was showed to mediate the SOX17 deficiency-induced EC dysfunction. Pharmacological inhibition of E2F1 in ecKO Sox17 mice attenuated PH and cell cycle programming. Our study demonstrated that endothelial SOX17 deficiency induces PH through E2F1 and targeting E2F1 signaling represents a promising approach in PAH patients.

2023-06-27 | GSE218398 | GEO

E2F1 mediates SOX17 Deficiency-Induced Pulmonary Hypertension [scRNA-seq]

Project description:E2F1 mediates SOX17 Deficiency-Induced Pulmonary Hypertension [scRNA-seq]

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CRISPR and siRNA manipulation of SOX17 in human pulmonary artery endothelial cells HPAEC

Project description:HPAEC were treated with either siRNA to SOX17 or CRISPR activating or inhibiting the promoter or an enhancer region associated with pulmonary hypertension and sequenced.

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Hypoxic pulmonary hypertension study

Project description:These microarray studies were performed using whole lungs of BALB/C mice during development of hypoxia-induced pulmonary hypertension (days 1-21) and resolution of pulmonary hypertension after return to normoxia (days 22-35) . Mice were sampled during nine time-points and each time-point was replicated 4 times (with dye swapping). Keywords = hypoxia Keywords = pulmonary hypertension

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