Axonal protection by brimonidine with modulation of p62 expression in TNF-induced optic nerve degeneration

التفاصيل البيبلوغرافية
العنوان: Axonal protection by brimonidine with modulation of p62 expression in TNF-induced optic nerve degeneration
المؤلفون: Kana Sase, Kaori Kojima, Hitoshi Takagi, Yasushi Kitaoka, Yasunari Munemasa
المصدر: Graefe's Archive for Clinical and Experimental Ophthalmology
بيانات النشر: Springer Science and Business Media LLC, 2015.
سنة النشر: 2015
مصطلحات موضوعية: Male, Pathology, medicine.medical_specialty, Tumor necrosis factor, Optic nerve, Immunoblotting, Axonal loss, Cell Count, Immunoenzyme Techniques, Cellular and Molecular Neuroscience, Sequestosome 1, Basic Science, Brimonidine Tartrate, Optic Nerve Diseases, Sequestosome-1 Protein, Adrenergic alpha-2 Receptor Agonists, Autophagy, medicine, Animals, Rats, Wistar, education, Heat-Shock Proteins, education.field_of_study, Tumor Necrosis Factor-alpha, business.industry, Brimonidine, p62, Axons, Sensory Systems, Rats, Disease Models, Animal, Ophthalmology, medicine.anatomical_structure, Retinal ganglion cell, Anesthesia, Intravitreal Injections, Nerve Degeneration, Tumor necrosis factor alpha, business, medicine.drug
الوصف: Purpose The p62, also called sequestosome 1 (SQSTM1), plays a crucial role in tumor necrosis factor (TNF)-induced optic nerve degeneration. Brimonidine has been shown to have protective effects on retinal ganglion cell bodies, although its role in their axons remains to be examined. We determined whether brimonidine modulates axonal loss induced by TNF and affects the expression of p62 in the optic nerve. Methods Experiments were performed on adult male Wistar rats that received an intravitreal injection of 10 ng TNF alone or simultaneous injection of TNF and 2, 20, or 200 pmol of brimonidine tartrate. The expression of p62 in the optic nerve was examined by immunoblot analysis. The effects of brimonidine on axons were evaluated by counting axon numbers 2 weeks after intravitreal injection. Results Intravitreal injection of brimonidine exerted substantial axonal protection against TNF-induced optic nerve degeneration. Immunoblot analysis showed that p62 was upregulated in the optic nerve after intravitreal injection of TNF, and that this increase was completely inhibited by brimonidine. Treatment with brimonidine alone also significantly decreased p62 protein levels in the optic nerve compared with the basal level. Conclusions These results suggest that the modulation of p62 levels in the optic nerve by brimonidine may be involved partly in its axonal protection.
تدمد: 1435-702X
0721-832X
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::01ee7864cd393d138f090d5b535a7722Test
https://doi.org/10.1007/s00417-015-3005-3Test
حقوق: OPEN
رقم الانضمام: edsair.doi.dedup.....01ee7864cd393d138f090d5b535a7722
قاعدة البيانات: OpenAIRE