Increased expression of the proton-sensing G protein-coupled receptor Gpr65 during retinal degeneration
| Autor: | Brigitte Kast, Marijana Samardzija, Christian Caprara, Divya Ail, V. Rüfenacht, Christian Grimm |
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| Přispěvatelé: | University of Zurich, Grimm, C |
| Rok vydání: | 2015 |
| Předmět: |
10018 Ophthalmology Clinic
Retinal degeneration Light microglia Mice Transgenic Nerve Tissue Proteins 610 Medicine & health Degeneration (medical) Biology Retina Receptors G-Protein-Coupled Mice 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Gpr65 TDAG8 Electroretinography medicine Animals RNA Messenger Eye Proteins Receptor rd10 030304 developmental biology G protein-coupled receptor Analysis of Variance 0303 health sciences Microglia General Neuroscience 2800 General Neuroscience Retinal Anatomy light damage medicine.disease Cell biology Mice Inbred C57BL Disease Models Animal medicine.anatomical_structure Gene Expression Regulation chemistry retinal degeneration Cytokines sense organs 030217 neurology & neurosurgery Homeostasis |
| Zdroj: | Neuroscience |
| ISSN: | 0306-4522 |
| DOI: | 10.1016/j.neuroscience.2015.06.039 |
| Popis: | The retina is a metabolically highly active tissue that is sensitive to pH changes. Blinding diseases of the retina are often characterized by degeneration of photoreceptor cells altering the acid-base homeostasis of the tissue microenvironment and by an accompanying inflammatory response. GPR4, GPR65 and GPR68 are G protein-coupled receptors that aid cells to sense and survive conditions of acidic pH and inflammatory cells express Gpr65 enhancing their viability. Hence, we investigated expression and function of these proton-sensing GPRs in the normal and degenerating retina. We observed increased retinal expression of Gpr65 , but not of Gpr4 and Gpr68 , in mouse models of both inherited ( rd10 ) and induced (light damage) retinal degeneration. Lack of GPR65 slightly accelerated photoreceptor degeneration in rd10 mice and resulted in a strong activation of microglia after light-injury. Since GPR65 was dispensable for normal retinal development, function and aging as evidenced by the evaluation of Gpr65 −/− mice, our results indicate that the proton-sensing G protein-coupled receptor GPR65 may be involved in a mechanism that supports survival of photoreceptors in the degenerating retina. |
| Databáze: | OpenAIRE |
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