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

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

PROVIDER: PRJNA436550 | ENA |

REPOSITORIES: ENA

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

Project description:Macrophage aging is pathogenic in numerous age-associated diseases, including age-related macular degeneration. The purpose of this experiment was to profile microRNA expression in young and aged macrophages at baseline and in response to oxLDL and acLDL.

2018-04-05 | GSE111304 | GEO

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.

2018-04-05 | GSE111322 | GEO

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

| PRJNA436592 | ENA

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

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

| PRJNA436587 | ENA

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

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-04-05 | GSE111323 | GEO

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.

| S-EPMC5928865 | biostudies-literature

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.

2024-10-31 | GSE271038 | GEO

Macular Degeneration

Project description:Age-related macular degeneration has a strong epidemiological association with cardiovascular disease. One pathogenic hypothesis that applies to both diseases is the concept of an abnormal cellular response to injury resulting in a disease phenotype. It has been hypothesized that this phenotype is also present in dermal fibroblasts. This study tests this hypothesis by examination of the expression profiles of fibroblasts obtained from diseased patients and subjected to sublethal cell injury. Keywords: other

2004-09-02 | GSE1719 | GEO

Epigenetic Regulation of IL17RC in Age-related Macular Degeneration

Project description:This SuperSeries is composed of the following subset Series: GSE28002: Gene expression of the whole mouse eye GSE28032: Epigenetic Regulation of IL17RC in Age-related Macular Degeneration (MeDIP-chip) Refer to individual Series

2011-03-22 | E-GEOD-28033 | biostudies-arrayexpress

Single-cell analysis reveals inflammatory interactions driving macular degeneration

Project description:Due to commonalities in pathophysiology, age-related macular degeneration represents a uniquely accessible model to investigate therapies for neurodegenerative diseases, leading us to examine whether pathways of disease progression are shared across neurodegenerative conditions. Here we use single-nucleus RNA sequencing to profile lesions from 17 retinas with age-related macular degeneration and controls. We create a machine learning pipeline based on recent advances in data geometry and topology and identify activated glial populations enriched in the early phase of disease. Examining single-cell data from Alzheimer’s disease and progressive multiple sclerosis with our pipeline, we find a similar glial activation profile enriched in the early phase of these neurodegenerative diseases. In late-stage age-related macular degeneration, we identify a microglia-to-astrocyte signaling axis mediated by interleukin-1beta which drives angiogenesis characteristic of disease pathogenesis. Thus, due to shared glial states, the retina provides a system for investigating therapeutic approaches in neurodegenerative diseases.

2023-01-18 | GSE221042 | GEO

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