کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6272163 | 1614775 | 2015 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Increased expression of the proton-sensing G protein-coupled receptor Gpr65 during retinal degeneration
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Increased expression of the proton-sensing G protein-coupled receptor Gpr65 during retinal degeneration Increased expression of the proton-sensing G protein-coupled receptor Gpr65 during retinal degeneration](/preview/png/6272163.png)
چکیده انگلیسی
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 Gpr65â/â 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.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 301, 20 August 2015, Pages 496-507
Journal: Neuroscience - Volume 301, 20 August 2015, Pages 496-507
نویسندگان
D. Ail, V. Rüfenacht, C. Caprara, M. Samardzija, B. Kast, C. Grimm,