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Single-cell transcriptomics of mouse lung lymphatic endothelial cells

ABSTRACT: Single-cell transcriptomics of mouse lung lymphatic endothelial cells

PROVIDER: PRJNA882365 | ENA |

REPOSITORIES: ENA

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Single-cell transcriptomics of mouse lung lymphatic endothelial cells

Project description:Fluid clearance mediated by lymphatic vessels is known to be essential for lung inflation and gas exchange function during the transition from prenatal to postnatal life, yet the molecular mechanisms that regulate lymphatic function remain unclear. Here, we profiled the molecular features of lymphatic endothelial cells (LECs) in embryonic and postnatal day (P) 0 lungs by single-cell RNA-seq analysis. We identified that the expression of c-JUN is transiently upregulated in P0 LECs. Conditional knockout of Jun in LECs impairs the opening of lung lymphatic vessels at birth, leading to fluid retention in the lungs and neonatal death. We further demonstrated that increased mechanical pressure induces the expression of c-JUN in LECs. c-JUN regulates the opening of lymphatic vessels by modulating remodeling of the actin cytoskeleton in LECs. Our study established the essential regulatory function of c-JUN-mediated transcriptional responses in facilitating lung lymphatic fluid clearance at birth.

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Project description:Tissue lymphatic vessels network plays critical roles in immune surveillance and tissue homeostasis in response to pathogen invasion, but how lymphatic system per se is remolded during infection is less understood. Here, we observed that influenza infection induces a significant increase of lymphatic vessel numbers in the lung, accompanied with extensive proliferation of lymphatic endothelial cells (LECs). Single-cell RNA sequencing illustrated the heterogeneity of LECs, identifying a novel PD-L1+ subpopulation that is present during viral infection but not at steady state. Specific deletion of Pd-l1 in LECs elevated the expansion of lymphatic vessel numbers during viral infection. Together these findings elucidate a dramatic expansion of lung lymphatic network in response to viral infection, and reveal a PD-L1+ LEC subpopulation that potentially modulates lymphatic vessel remolding.

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Project description:We examined transcriptional remodeling of lymph node lymphatic endothelial cells in response to imiquimod-induced inflammation using single-cell RNA sequencing.

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Project description:Using single-cell RNA sequencing, we provide a comprehensive map of lymph node resident lymphatic endothelial cells, identifying subpopulations, new markers and functions.

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mouse lung endothelial single cell transcriptomics

Project description:Disruption of pulmonary vascular homeostasis is a central feature of viral pneumonia, wherein endothelial cell (EC) death and subsequent angiogenic responses represent critical determinants of the outcome of severe lung injury. A more granular understanding of the fundamental mechanisms driving reconstitution of the lung endothelium is necessary to facilitate therapeutic targeting of vascular repair. Here, we applied single-cell RNA sequencing (scRNA-seq) to profile lung ECs from mice on D0, D20 and D30 post influenza infection. Our data revealed the dynamics of endothelial subsets during influenza injury.

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