ArticlePloS one2012
Post-translational processing of synaptophysin in the rat retina is disrupted by diabetes.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 32 citations in OpenAlex.
- Anatolian ground squirrel (Spermophilus xanthoprymnus) retina: Comparative expression of synaptophysin, NeuN, calbindin-D28k, parvalbumin, glial fibrillary acidic protein, and Iba-1 during pre-hibernation and hibernation.Anatomical record (Hoboken, N.J. : 2007) · 2026Article
- Review
- Association Between Macular Ganglion Cell-Inner Plexiform Layer and Non-Proliferative Retinopathy Without Macular Edema in Type 2 Diabetes via Diabetes Duration and HbABiomedicines · 2025Article
- Article
- Therapeutic effects of tetrahedral framework nucleic acids and tFNAs-miR22 on retinal ischemia/reperfusion injury.Cell proliferation · 2024Article
- Posttranslational modifications of proteins in diseased retina.Frontiers in cellular neuroscience · 2023Review
- The Pathogenesis and Therapeutic Approaches of Diabetic Neuropathy in the Retina.International journal of molecular sciences · 2021Review
- Treatment of diabetic retinopathy through neuropeptide Y-mediated enhancement of neurovascular microenvironment.Journal of cellular and molecular medicine · 2020Article
- Loss of XBP1 Leads to Early-Onset Retinal Neurodegeneration in a Mouse Model of Type I Diabetes.Journal of clinical medicine · 2019Article
- Retinal Neurodegeneration as an Early Manifestation of Diabetic Eye Disease and Potential Neuroprotective Therapies.Current diabetes reports · 2019Review
- The neurovascular unit and the pathophysiologic basis of diabetic retinopathy.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2017Review
- Pituitary Adenylate Cyclase Activating Polypeptide, A Potential Therapeutic Agent for Diabetic Retinopathy in Rats: Focus on the Vertical Information Processing Pathway.Neurotoxicity research · 2016Article
- Neuroprotection as a Therapeutic Target for Diabetic Retinopathy.Journal of diabetes research · 2016Review
- Retinal Failure in Diabetes: a Feature of Retinal Sensory Neuropathy.Current diabetes reports · 2015Review
- Association of chromosome 5q21.3 polymorphisms with the exploratory eye movement dysfunction in schizophrenia.Scientific reports · 2015Article
- High-fat diet ingestion correlates with neuropathy in the duodenum myenteric plexus of obese mice with symptoms of type 2 diabetes.Cell and tissue research · 2013Article
- Neuroprotective Effects of Human Adipose-Derived Mesenchymal Stem Cells in Oxygen-Induced Retinopathy.Cell transplantationArticle
- Diabetes and retinal vascular dysfunction.Journal of ophthalmic & vision researchReview
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4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Synaptophysin, is an abundant presynaptic protein involved in synaptic vesicle recycling and neurotransmitter release. Previous work shows that its content is significantly reduced in the rat retina by streptozotocin (STZ)-diabetes. This study tested the hypothesis that STZ-diabetes alters synaptophysin protein turnover and glycosylation in the rat retina. Whole explant retinas from male Sprague-Dawley rats were used in this study. Rats were made diabetic by a single intraperitoneal STZ injection (65 mg/kg body weight in 10 mM sodium citrate, pH 4.5). mRNA translation was measured using a (35)S-methionine labeling assay followed by synaptophysin immunoprecipitation and autoradiography. A pulse-chase study was used to determine the depletion of newly synthesized synaptophysin. Depletion of total synaptophysin was determined after treatment with cycloheximide. Mannose rich N-glycosylated synaptophysin was detected by treating retinal lysates with endoglycosidase H followed by immunoblot analysis. Synaptophysin mRNA translation was significantly increased after 1 month (p<0.001) and 2 months (p<0.05) of STZ-diabetes, compared to age-matched controls. Newly synthesized synaptophysin degradation was significantly accelerated in the retina after 1 and 2 months of diabetes compared to controls (p<0.05). Mannose rich glycosylated synaptophysin was significantly increased after 1 month of STZ-diabetes compared to controls (p<0.05).These data suggest that diabetes increases mRNA translation of synaptophysin in the retina, resulting in an accumulation of mannose rich glycosylated synaptophysin, a transient post-translational state of the protein. This diabetes-induced irregularity in post-translational processing could explain the accelerated degradation of retinal synaptophysin in diabetes.
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