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Transcriptome changes associated with targeting mTORC1 in endothelial cells

ABSTRACT: Transcriptome changes associated with targeting mTORC1 in endothelial cells

PROVIDER: PRJNA1079803 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28074532_1.fastq.gz	Fastqsanger.gz
	SRR28074532_2.fastq.gz	Fastqsanger.gz
	SRR28074533_1.fastq.gz	Fastqsanger.gz
	SRR28074533_2.fastq.gz	Fastqsanger.gz
	SRR28074534_1.fastq.gz	Fastqsanger.gz

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Transcriptome changes associated with targeting mTORC1 in endothelial cells

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Hyperactive mTORC1 in Lung Mesenchyme Induces Endothelial Cell Dysfunction and Pulmonary Vascular Remodeling

Project description:Lymphangioleiomyomatosis (LAM) is a progressive cystic lung disease caused by tuberous sclerosis complex 1/2 (TSC1/2) gene mutations resulting in activation of the mechanistic target of rapamycin complex 1 (mTORC1). A subset of LAM patients develops pulmonary vascular remodeling and pulmonary hypertension. To model LAM disease, we utilized an mTORC1 gain-of-function mouse model with a Tsc2 knock-out (Tsc2KO) specific to lung mesenchyme (Tbx4LME-CreTsc2fl/fl), similar to the mesenchyme specific genetic alterations seen in human disease. As early as 8 weeks of age, ECs from Tbx4LME-CreTsc2fl/fl mice exhibited marked transcriptomic changes despite absence of morphological changes to the distal lung microvasculature. In contrast, 1 year old Tbx4LME-CreTsc2fl/fl mice spontaneously developed pulmonary vascular remodeling with increased medial thickness. We subsequently performed single cell RNA-sequencing of 1 year old mouse lung and identified paracrine ligands originating from Tsc2KO mesenchyme impacting arterial endothelial cells. These cells contained transcriptionally altered genes including those in pathways associated with blood vessel remodeling, highlighting the pathogenic importance of the mesenchymal-endothelial cell axis.

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