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Proteasome Stress in Skeletal Muscle Mounts a Long-Range Protective Response that Delays Retinal and Brain Aging [Drosophila]

ABSTRACT: Proteasome Stress in Skeletal Muscle Mounts a Long-Range Protective Response that Delays Retinal and Brain Aging [Drosophila]

PROVIDER: PRJNA630174 | ENA |

REPOSITORIES: ENA

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Proteasome Stress in Skeletal Muscle Mounts a Long-Range Protective Response that Delays Retinal and Brain Aging

Project description:Proteasome Stress in Skeletal Muscle Mounts a Long-Range Protective Response that Delays Retinal and Brain Aging

| PRJNA630171 | ENA

Proteasome Stress in Skeletal Muscle Mounts a Long-Range Protective Response that Delays Retinal and Brain Aging [Human]

Project description:Proteasome Stress in Skeletal Muscle Mounts a Long-Range Protective Response that Delays Retinal and Brain Aging [Human]

| PRJNA630173 | ENA

Proteasome Stress in Skeletal Muscle Mounts a Long-Range Protective Response that Delays Retinal and Brain Aging [Human]

Project description:The proteasome maintains protein quality during aging and disease. Challenges to proteasome function can be compensated by local proteasome stress responses. However, whereas proteasome stress is also sensed systemically is unknown. In Drosophila , we find that proteasome stress in skeletal muscle non-autonomously promotes the degradation of proteasome substrates in distant tissues during aging. Several muscle-secreted factors (myokines) are upregulated by proteasomal stress via C/EBP transcription factors, including the amylase Amyrel, which increases the circulating levels of the disaccharide maltose. Muscle-specific Amyrel overexpression promotes the degradation of proteasome substrates in the aging brain and retina via the transcriptional induction of chaperones and proteases. Conversely, RNAi for maltose transporters worsens proteostasis and reduces the expression of Amyrel-induced genes in the brain. Moreover, maltose preserves protein quality in cell culture and human cortical brain organoids challenged by thermal stress. Thus, proteasome stress in skeletal muscle mounts a systemic adaptive response via amylase/maltose signaling.

2021-02-12 | GSE149797 | GEO

Proteasome Stress in Skeletal Muscle Mounts a Long-Range Protective Response that Delays Retinal and Brain Aging [Drosophila]

2021-02-12 | GSE149798 | GEO

Proteasome Stress in Skeletal Muscle Mounts a Long-Range Protective Response that Delays Retinal and Brain Aging

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

2021-02-12 | GSE149799 | GEO

Transcriptomic analysis of transferrin protective effect during retinal detachment in mice

Project description:Transcriptomic analysis of transferrin protective effect during retinal detachment in mice.

2019-08-31 | GSE102824 | GEO

Interleukin-17-Mediated Protective Cytokine Signaling Against Degeneration of the Retinal Pigment Epithelium

Project description:Injuries to the retinal pigment epithelium (RPE) and outer retina often result in the accumulation of retinal microglia within the subretinal space. These subretinal microglia play crucial roles in inflammation and resolution, but the mechanisms governing their functions are still largely unknown. Our previous research highlighted the protective functions of choroidal gd T cells in response to RPE injury. In the current study, we employed single-cell RNA sequencing approach to delve deeper into the mechanisms involved. We found that gd T cells were the primary producer of interleukin-17 (IL-17) in the choroid. IL-17 signaled through its receptor on the RPE, subsequently triggering the production of interleukin-6 (IL-6). This cascade of cytokines initiated a metabolic reprogramming of subretinal microglia, enhancing their capacity for lipid metabolism. RPE-specific knockout of IL-17 receptor A led to the dysfunction of subretinal microglia and RPE pathology. Collectively, our findings suggest that responding to RPE injury, the choroidal gd T cells can initiate a protective signaling cascade that ensures the proper functioning of subretinal microglia.

2023-11-29 | GSE244661 | GEO

Modifications in Retinal Microvascularization With Targeted Anti-angiogenic Therapy in Colorectal Cancer

Project description:Retinal microvascularization can provide important informations to systemic vascular phenomena. The non-invasive quantitative description of the retinal vascularization is now possible by performing OCT-angiography and their image analysis software (vascular density and retinal perfusion). Systemic microvacular changes during the establishment of oncological treatment by targeted antiangiogenic therapy are little described in the literature. The objective of this pilot study is to describe the evolution of the retinal vascular density of patients with antiangiogenic drugs. In addition, the evolution of the retinal vascular density of patients on antiangiogenic drugs will study as a function of the response to the treatment and the toxicity of these treatments.

| 2382594 | ecrin-mdr-crc

Aldose reductase inhibition decelerates optic nerve degeneration by suppressing retinal microglia activation

Project description:To investigate the role of aldose reductase (AR) inhibition using Sorbinil on retinal microglia (RMG) activation, retinal ganglion cell (RGC) survival, and axon regeneration after optic nerve trauma. We observed that AR inhibition using Sorbinil attenuates RMG activation and subsequently promotes RGC survival and delays axon degeneration one week after optic nerve crush.

2023-04-05 | GSE200233 | GEO

Genetic targeting or pharmacological inhibition of galectin-3 dampens microglia reactivity and delays retinal degeneration

Project description:Dysfunctional humoral and cellular innate immunity are key components in the development and progression of age-related macular degeneration (AMD). Specifically, chronically activated microglia and their disturbed regulatory system contribute to retinal degeneration. Galectin-3, a b-galactose binding protein, is a potent driver of macrophage and microglia activation and has been implicated in neuroinflammation, including neurodegenerative diseases of the brain. Here, we report that galectin-3 is strongly upregulated in reactive retinal microglia of AMD patients and in two related mouse models of retinal degeneration. Specific targeting of galectin-3 by genetic knockout or using the small-molecule inhibitor TD139 blocks microglia reactivity and protects from retinal damage in different models of light-induced retinal degeneration. These data define galectin-3 as potent driver of retinal degeneration and highlight the protein as a drug target for ocular immunomodulatory therapies.

2022-08-15 | GSE211119 | GEO

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