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转导蛋白 1、光转导与早期糖尿病性视网膜病变的发生。

Transducin1, Phototransduction and the Development of Early Diabetic Retinopathy.

机构信息

Department of Biology, Case Western Reserve University, Cleveland, Ohio, United States.

Department of Pharmacology, Case Western Reserve University, Cleveland, Ohio, United States.

出版信息

Invest Ophthalmol Vis Sci. 2019 Apr 1;60(5):1538-1546. doi: 10.1167/iovs.18-26433.

DOI:10.1167/iovs.18-26433
PMID:30994864
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6736377/
Abstract

PURPOSE

Recent evidence suggests that retinal photoreceptor cells have an important role in the pathogenesis of retinal microvascular lesions in diabetes. We investigated the role of rod cell phototransduction on the pathogenesis of early diabetic retinopathy (DR) using Gnat1-/- mice (which causes permanent inhibition of phototransduction in rod cells without degeneration).

METHODS

Retinal thickness, oxidative stress, expression of inflammatory proteins, electroretinograms (ERG) and optokinetic responses, and capillary permeability and degeneration were evaluated at up to 8 months of diabetes.

RESULTS

The diabetes-induced degeneration of retinal capillaries was significantly inhibited in the Gnat1-/- diabetics. The effect of the Gnat1 deletion on the diabetes-induced increase in permeability showed a nonuniform accumulation of albumin in the neural retina; the defect was inhibited in diabetic Gnat1-/- mice in the inner plexiform layer (IPL), but neither in the outer plexiform (OPL) nor inner nuclear (INL) layers. In Gnat1-deficient animals, the diabetes-induced increase in expression of inflammatory associated proteins (iNOS and ICAM-1, and phosphorylation of IĸB) in the retina, and the leukocyte mediated killing of retinal endothelial cells were inhibited, however the diabetes-mediated induction of oxidative stress was not inhibited.

CONCLUSIONS

In conclusion, deletion of transducin1 (and the resulting inhibition of phototransduction in rod cells) inhibits the development of retinal vascular pathology in early DR.

摘要

目的

最近的证据表明，视网膜光感受器细胞在糖尿病性视网膜微血管病变的发病机制中起着重要作用。我们使用 Gnat1-/- 小鼠（可永久性抑制视杆细胞的光转导而不引起变性）研究了视杆细胞光转导在早期糖尿病视网膜病变（DR）发病机制中的作用。

方法

在糖尿病长达 8 个月时，评估视网膜厚度、氧化应激、炎症蛋白表达、视网膜电图（ERG）和视动反应以及毛细血管通透性和变性。

结果

Gnat1-/- 糖尿病小鼠中，糖尿病引起的视网膜毛细血管变性明显受到抑制。Gnat1 缺失对糖尿病引起的通透性增加的影响表现为白蛋白在神经视网膜中的非均匀积累；在糖尿病 Gnat1-/- 小鼠中，内丛状层（IPL）中的缺陷被抑制，但在外丛状层（OPL）和内核层（INL）中均未被抑制。在 Gnat1 缺陷型动物中，糖尿病引起的视网膜中炎症相关蛋白（iNOS 和 ICAM-1 以及 IκB 磷酸化）表达增加，以及白细胞介导的视网膜内皮细胞杀伤作用受到抑制，但糖尿病介导的氧化应激诱导并未受到抑制。

结论

总之，转导蛋白 1 的缺失（并导致视杆细胞的光转导抑制）抑制了早期 DR 中视网膜血管病理的发展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd40/6736377/6925889e333f/i1552-5783-60-5-1538-f07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd40/6736377/8d9d570601b1/i1552-5783-60-5-1538-f01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd40/6736377/d2c63d694304/i1552-5783-60-5-1538-f02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd40/6736377/5c1943fab0f8/i1552-5783-60-5-1538-f03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd40/6736377/eb6757b17a36/i1552-5783-60-5-1538-f04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd40/6736377/16343e0ffe65/i1552-5783-60-5-1538-f05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd40/6736377/7d8a39f2a6f9/i1552-5783-60-5-1538-f06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd40/6736377/6925889e333f/i1552-5783-60-5-1538-f07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd40/6736377/8d9d570601b1/i1552-5783-60-5-1538-f01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd40/6736377/d2c63d694304/i1552-5783-60-5-1538-f02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd40/6736377/5c1943fab0f8/i1552-5783-60-5-1538-f03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd40/6736377/eb6757b17a36/i1552-5783-60-5-1538-f04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd40/6736377/16343e0ffe65/i1552-5783-60-5-1538-f05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd40/6736377/7d8a39f2a6f9/i1552-5783-60-5-1538-f06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd40/6736377/6925889e333f/i1552-5783-60-5-1538-f07.jpg

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