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Glucocorticoid Regulates Mesenchymal Cell Differentiation Required for Perinatal Lung Morphogenesis and Function

ABSTRACT: Glucocorticoid Regulates Mesenchymal Cell Differentiation Required for Perinatal Lung Morphogenesis and Function

PROVIDER: PRJNA564113 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10074949_1.fastq.gz	Fastqsanger.gz
	SRR10074949_2.fastq.gz	Fastqsanger.gz
	SRR10074950_1.fastq.gz	Fastqsanger.gz
	SRR10074950_2.fastq.gz	Fastqsanger.gz
	SRR10074951_1.fastq.gz	Fastqsanger.gz

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Glucocorticoid Regulates Mesenchymal Cell Differentiation Required for Perinatal Lung Morphogenesis and Function

Project description:We integrated genome-wide gene expression profiling, ATAC-seq, and single cell RNA-seq data in mice in which GR was deleted or activated to identify the cellular and molecular mechanisms by which glucocorticoids control prenatal lung maturation. GR activated differentiation of a newly defined proliferative mesenchymal progenitor cell (PMP) into matrix fibroblasts (MFB), in part by directly activating extracellular matrix-associated target genes, including Fn1, Col16a4, and Eln and modulating FGF, VEGF, JAK-STAT and WNT signaling. Loss of mesenchymal GR signaling blocked PMP differentiation into mature MFB, which in turn caused proliferation of SOX9+ alveolar epithelial progenitor cells and inhibited differentiation of more mature AT2 and AT1 cells. GR signaling controls genes required for differentiation of a subset of proliferative mesenchymal progenitors into matrix fibroblasts in turn, regulating signals controlling AT2/AT1 progenitor cell proliferation and differentiation, identifying cells and processes by which glucocorticoid signaling regulates fetal lung function.

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Glucocorticoid regulates mesenchymal cell differentiation required for perinatal lung morphogenesis and function.

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