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PDZK1 Protects Against RPE Senescence by Targeting the 14-3-3ε-mTOR Axis to Attenuate Early Diabetic Retinopathy

ABSTRACT: PDZK1 Protects Against RPE Senescence by Targeting the 14-3-3ε-mTOR Axis to Attenuate Early Diabetic Retinopathy

PROVIDER: PRJNA1301643 | ENA |

REPOSITORIES: ENA

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PDZK1 Protects Against RPE Senescence by Targeting the 14-3-3ε-mTOR Axis to Attenuate Early Diabetic Retinopathy

Project description:In diabetic retinopathy (DR), hyperglycemia induces retinal pigment epithelium (RPE) cell senescence via downregulation of PDZK1. PDZK1 overexpression counteracts senescence by binding 14-3-3ε to modulate mTOR signaling, reducing oxidative stress and enhancing autophagy. Both genetic PDZK1 restoration and pharmacologic senolysis (Nutlin-3a) attenuate retinal senescence and ameliorate early DR pathology, establishing the PDZK1-14-3-3ε-mTOR axis as a therapeutic target

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PDZK1 Protects Against RPE Senescence by Targeting the 14-3-3ε-mTOR Axis to Attenuate Early Diabetic Retinopathy [MG_HG]

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PDZK1 Protects Against RPE Senescence by Targeting the 14-3-3ε-mTOR Axis to Attenuate Early Diabetic Retinopathy [MG_HG]

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Extensive Sub-RPE Complement Deposition in a Nonhuman Primate Model of Early Stage Diabetic Retinopathy

Project description:Purpose: This study aims to reveal retinal abnormities in a spontaneous diabetic nonhuman primate (NHP) model and explore the mechanism of featured injuries. Methods: Twenty-eight cynomolgus monkeys were identified to suffer from spontaneous Type 2 diabetes from a colony of more than eight hundred aged monkeys and twenty-six age-matched ones were used as controls. Their blood biochemistry profiles were determined and the retinal changes were examined by multimodal imaging, hematoxylin-eosin (H&E) staining and immunofluorescence. Retinal pigment epithelium (RPE) cells were isolated and determined by RNA-sequencing and computational analyses. Results: Diabetic monkeys were characterized by early vascular and neural damage in the retina and dyslipidemia. The typical acellular capillaries and pericyte ghost were found in the diabetic retina, which also exhibited reduced retinal nerve fiber layer (RNFL) thickness compared to the controls. Of note, distinct sub-RPE drusenoid lesions were extensively observed in these diabetic monkeys and complements deposition including C3 and C5b-9 were accumulated in these lesions. The RNA-seq data of RPE cells showed complement activation, AGE/RAGE activation and 18 inflammatory response at the setting of diabetes. Consistently, the plasma levels of C3 and C4 were also increased in the diabetic monkeys. Conclusions: The spontaneous Type 2 diabetic cynomolgus monkeys featured with early-stage retinopathy including not only typical vascular and neural damage, but also a distinct sub-RPE deposition. The complement activation and metabolic stress of RPE cells in response to hyperglycemia might contribute to the deposition, revealing an unrecognized role of RPE cells in the early-stage pathological process of diabetic retinopathy (DR).

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Incipient diabetic retinopathy - Early regulation of genes

Project description:The development of diabetic retinopathy is well characterized on a histological level. Early vascular alterations involve the loss of pericytes. Earlier mechanisms leading to the phenotype of diabetic retinopathy, which involves the complete neurovascular unit, are not yet fully understood. The gene expression data presented here is derived from microarrays and gives further insights into early genetic regulation in incipient diabetic retinopathy.

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mTOR activity is essential for retinal pigment epithelium regeneration in zebrafish

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Extensive Sub-RPE Complement Deposition in a Nonhuman Primate Model of Early Stage Diabetic Retinopathy

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Cellular and Molecular Linkage between Diabetic Nephropathy and Diabetic Retinopathy

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