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Macrophage microRNA-150 promotes pathological angiogenesis as seen in age-related macular degeneration

ABSTRACT: Macrophage microRNA-150 promotes pathological angiogenesis as seen in age-related macular degeneration

PROVIDER: PRJNA436587 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6796210.fastq.gz	Fastqsanger.gz
	SRR6796220.fastq.gz	Fastqsanger.gz
	SRR6796211.fastq.gz	Fastqsanger.gz
	SRR6796221.fastq.gz	Fastqsanger.gz
	SRR6796212.fastq.gz	Fastqsanger.gz

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Macrophage microRNA-150 promotes pathological angiogenesis as seen in age-related macular degeneration: part II

Project description:Macrophage microRNA-150 promotes pathological angiogenesis as seen in age-related macular degeneration: part II

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Macrophage microRNA-150 promotes pathological angiogenesis as seen in age-related macular degeneration: part I

Project description:Macrophage microRNA-150 promotes pathological angiogenesis as seen in age-related macular degeneration: part I

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Macrophage microRNA-150 promotes pathological angiogenesis as seen in age-related macular degeneration: part I

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Macrophage microRNA-150 promotes pathological angiogenesis as seen in age-related macular degeneration: part II

Project description:We identified that microRNA-150 is upregulated in aged macrophages of diverse origins and therefore may mechanistically skew them towards a disease-promoting phenotype. The purpose of this experiment was to identify how the murine transcriptome changes with microRNA-150 overexpression.

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Macrophage microRNA-150 promotes pathological angiogenesis as seen in age-related macular degeneration.

Project description:Macrophage aging is pathogenic in diseases of the elderly, including age-related macular degeneration (AMD), a leading cause of blindness in older adults. However, the role of microRNAs, which modulate immune processes, in regulating macrophage dysfunction and thereby promoting age-associated diseases is underexplored. Here, we report that microRNA-150 (miR-150) coordinates transcriptomic changes in aged murine macrophages, especially those associated with aberrant lipid trafficking and metabolism in AMD pathogenesis. Molecular profiling confirmed that aged murine macrophages exhibit dysregulated ceramide and phospholipid profiles compared with young macrophages. Of translational relevance, upregulation of miR-150 in human peripheral blood mononuclear cells was also significantly associated with increased odds of AMD, even after controlling for age. Mechanistically, miR-150 directly targets stearoyl-CoA desaturase-2, which coordinates macrophage-mediated inflammation and pathologic angiogenesis, as seen in AMD, in a VEGF-independent manner. Together, our results implicate miR-150 as pathogenic in AMD and provide potentially novel molecular insights into diseases of aging.

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Macrophage microRNA-150 promotes pathological angiogenesis as seen in age-related macular degeneration

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Natural killer cells cooperate with neutrophils to suppress pathological angiogenesis in neovascular age-related macular degeneration

Project description:Neovascular age-related macular degeneration (nvAMD) is the leading cause of blindness in the elderly population associated with focal inflammation, however, understanding of the precise immune components governing this process is still limited. Here, we identified natural killer (NK) cells as a prominent lymphocyte population infiltrating the perivascular space of choroidal neovascularization (CNV) lesions. O-link analysis and single-cell RNA sequencing approaches identified CCR5-expressing NK cells is essential for further NK cell recruitment and extravasation in CNV site. NK cells suppress pathological angiogenesis via through clearance of senescent vasculatures, a process that requires neutrophil extracellular traps (NETs). Mechanistically, the release of NETs results from NKG2D-dependent NK cell activation and production of IFN-γ at CNV lesions. Notably , age is the strongest risk factor for AMD to an aged immune system; our human and mouse data showed that aged NK cells exhibited compromised protective effects. Additionally, expansion of NK cells by IL-2 complex improved CNV formation. Collectively, our results revealed a previously unrecognized role of NK cells in suppressing nvAMD progression, suggesting these cells as a potential target for future immune therapies for patients with nvAMD.

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Natural killer cells cooperate with neutrophils to suppress pathological angiogenesis in neovascular age-related macular degeneration

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