Thioredoxin delays photoreceptor degeneration, oxidative and inflammation alterations in retinitis pigmentosa
| Autor: | Antolin Cantó, Vicente Hernández-Rabaza, María Miranda, Roberto Gimeno-Hernández, Ángel Fernández-Carbonell, Teresa Olivar, Inmaculada Almansa |
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| Přispěvatelé: | Producción Científica UCH 2020, UCH. Departamento de Ciencias Biomédicas |
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
retina medicine.medical_specialty Programmed cell death Retinal Disorder glia medicine.medical_treatment Retinitis pigmentaria - Tratamiento Oxidative stress - Treatment 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine hepatic growth factor Internal medicine Retinitis pigmentosa medicine Pharmacology (medical) Crecimiento - Factores - Uso terapéutico glutathione Glutatión - Uso terapéutico Original Research Pharmacology Glutathione - Therapeutic use Retina Growth factors - Therapeutic use vascular endothelial growth factor Chemistry Retina - Diseases - Treatment Growth factor lcsh:RM1-950 Retinal thioredoxin Retinitis pigmentosa - Treatment medicine.disease eye diseases Vascular endothelial growth factor lcsh:Therapeutics. Pharmacology 030104 developmental biology Endocrinology medicine.anatomical_structure Estrés oxidativo - Tratamiento Tiorredoxina - Uso terapéutico sense organs Thioredoxin 030217 neurology & neurosurgery Thioredoxin - Therapeutic use Retina - Enfermedades - Tratamiento |
| Zdroj: | CEU Repositorio Institucional Fundación Universitaria San Pablo CEU (FUSPCEU) Frontiers in Pharmacology Frontiers in Pharmacology, Vol 11 (2020) |
| DOI: | 10.3389/fphar.2020.590572 |
| Popis: | Este artículo se encuentra disponible en la siguiente URL: https://www.frontiersin.org/articles/10.3389/fphar.2020.590572/full Retinitis pigmentosa (RP) is an inherited ocular disorder with no effective treatment. RP onset and progression trigger a cascade of retinal disorders that lead to the death of photoreceptors. After photoreceptors death, neuronal, glial and vascular remodeling can be observed in the retina. The purpose of this study was to study if thioredoxin (TRX) administration is able to decrease photoreceptor death in an animal model of RP (rd1 mouse), but also if it is able to modulate the retinal oxidative stress, glial and vascular changes that can be observed as the disease progresses. Wild type and rd1 mice received several doses of TRX. After treatment, animals were euthanized at postnatals days 11, 17, or 28. Glutathione (GSH) and other thiol compounds were determined by high performance liquid chromatography (HPLC). Glial fibrilary acidic protein (GFAP) and anti-ionized calcium binding adaptor molecule 1 (Iba1) were studied by immunohistochemistry. Vascular endothelial growth factor (VEGF) and hepatic growth factor (HGF) expression were determined by western blot. TRX administration significantly diminished cell death in rd1 mouse retinas and increased GSH retinal concentrations at postnatal day 11 (PN11). TRX was also able to reverse glial alterations at PN11 and PN17. No alterations were observed in retinal VEGF and HGF expression in rd1 mice. In conclusion, TRX treatment decreases photoreceptor death in the first stages of RP and this protective effect may be due in part to the GSH system activation and to a partially decrease in inflammation. |
| Databáze: | OpenAIRE |
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