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Regulation of brain endothelial cell physiology by the TAM receptor tyrosine kinase Mer

ABSTRACT: Regulation of brain endothelial cell physiology by the TAM receptor tyrosine kinase Mer

PROVIDER: PRJNA935761 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23499443.fastq.gz	Fastqsanger.gz
	SRR23499444.fastq.gz	Fastqsanger.gz
	SRR23499445.fastq.gz	Fastqsanger.gz
	SRR23499446.fastq.gz	Fastqsanger.gz
	SRR23499447.fastq.gz	Fastqsanger.gz

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Regulation of brain endothelial cell physiology by the TAM receptor tyrosine kinase Mer

Project description:The receptor tyrosine kinase Mer (gene name Mertk) acts in vascular endothelial cells (ECs) to tighten the blood-brain barrier (BBB) subsequent to viral infection. Correspondingly, we found that Mer regulates the expression and activity of a large cohort of cytoskeletal and BBB proteins, together with endothelial nitric oxide synthase, in brain ECs. We further found that Mer controls the expression of multiple angiogenic genes, and that EC-specific Mertk gene inactivation results in perturbed vascular sprouting and a compromised BBB after induced photothrombotic stroke. Unexpectedly, stroke lesions in the brain were also markedly reduced in the absence of EC Mer, which was linked to reduced plasma expression of fibrinogen, prothrombin, and other effectors of blood coagulation. Together, these results demonstrate that Mer is a central regulator of angiogenesis, BBB integrity, and blood coagulation in the mature vasculature. They may also account for disease severity following infection with the coronavirus SARS-CoV-2.

2023-08-24 | GSE225474 | GEO

Regulation of brain endothelial cell physiology by the TAM receptor tyrosine kinase Mer

2023-02-23 | MSV000091355 | MassIVE

The TAM receptor tyrosine kinases Axl and Mer drive the phagocytic differentiation of tissue-resident macrophages

Project description:Many apoptotic thymocytes are generated during the course of T cell selection in the thymus, yet the machinery through which these dead cells are recognized and phagocytically cleared is incompletely understood. We find that the TAM receptor tyrosine kinases Axl and Mer, which are co-expressed by a specialized set of phagocytic thymic macrophages, are essential components of this machinery. Axl-/-Mertk-/- double mutant mice exhibited a marked accumulation of apoptotic cells during the time that autoreactive and nonreactive thymocytes die. Unexpectedly, the double mutants also displayed a profound deficit in the total number of phagocytic macrophages in the thymus, and concomitantly exhibited diminished expression of key non-TAM engulfment systems in the macrophages that remain. These previously unrecognized deficits were not confined to the thymus, and were also evident in the bone marrow and spleen. They had pleiotropic metabolic consequences for the double mutants, which included severe dysregulation of hemoglobin turnover, iron metabolism, and erythropoiesis.

2022-07-12 | GSE192363 | GEO

The TAM receptor tyrosine kinases Axl and Mer drive the phagocytic differentiation of tissue-resident macrophages

Project description:The TAM receptor tyrosine kinases Axl and Mer drive the phagocytic differentiation of tissue-resident macrophages

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Regulation of brain endothelial cell physiology by the TAM receptor tyrosine kinase Mer.

Project description:The receptor tyrosine kinase Mer (gene name Mertk) acts in vascular endothelial cells (ECs) to tighten the blood-brain barrier (BBB) subsequent to viral infection, but how this is achieved is poorly understood. We find that Mer controls the expression and activity of a large cohort of BBB regulators, along with endothelial nitric oxide synthase. It also controls, via an Akt-Foxo1 pathway, the expression of multiple angiogenic genes. Correspondingly, EC-specific Mertk gene inactivation resulted in perturbed vascular sprouting and a compromised BBB after induced photothrombotic stroke. Unexpectedly, stroke lesions in the brain were also reduced in the absence of EC Mer, which was linked to reduced plasma expression of fibrinogen, prothrombin, and other effectors of blood coagulation. Together, these results demonstrate that Mer is a central regulator of angiogenesis, BBB integrity, and blood coagulation in the mature vasculature. They may also account for disease severity following infection with the coronavirus SARS-CoV-2.

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Tyrosine Kinase Inhibitor Cardiotoxicity

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Microglia use TAM receptors to detect and engulf amyloid beta plaques

Project description:Two microglial TAM receptor tyrosine kinases - Axl and Mer - have been linked to Alzheimer’s disease, but their roles in disease have not been tested experimentally. We find that in Alzheimer’s disease and its mouse models, induced expression of Axl and Mer in amyloid plaque-associated microglia is coupled to induced plaque decoration by the TAM ligand Gas6 and its co-ligand phosphatidylserine. In the APP/PS1 mouse model of Alzheimer’s disease, sIngle cell RNAseq analysis comparing wild type microglia with those with Axl and Mer deficiency reveals a similar disease state transitional program of microglia but a dampened differential expression of numerous AD siganture genes in microglia lacking TAM receptors. In line with the transcriptomic data, using two-photon microscopy, we show that genetic ablation of Axl and Mer results in microglia that are unable to normally detect, respond to, organize, or phagocytose amyloid beta plaques. These major deficits notwithstanding, and contrary to expectation, TAM-deficient APP/PS1 mice develop fewer dense-core plaques than APP/PS1 mice with normal microglia. Our findings reveal that the TAM system is an essential mediator of microglial recognition and engulfment of amyloid plaques, and that TAM-driven microglial phagocytosis does not constrain, but rather promotes, plaque development.

2021-02-25 | GSE160523 | GEO

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Yes tyrosine kinase signaling promotes liver cancer development

Project description:Yes tyrosine kinase signaling promotes liver cancer development

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