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Ctrp9(脂肪细胞因子 1 受体配体)缺失和小鼠视网膜中锥形光感受器数量减少。

Ablation of Ctrp9, Ligand of AdipoR1, and Lower Number of Cone Photoreceptors in Mouse Retina.

机构信息

Department of Ophthalmology, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Laboratory of Functional Genomics, Graduate School of Bioscience, Nagahama Institute of Bioscience and Technology, Shiga, Japan.

出版信息

Invest Ophthalmol Vis Sci. 2022 May 2;63(5):14. doi: 10.1167/iovs.63.5.14.

DOI:10.1167/iovs.63.5.14
PMID:35575905
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9123514/
Abstract

PURPOSE

C1q/TNF-related protein (CTRP) 9 is one of the adiponectin paralogs, and a genetic ablation of its receptor, AdipoR1, is known to cause retinal degeneration. The purpose of this study was to determine the role played by CTRP9 in the retina.

METHODS

The retinas of Ctrp9 gene knockout (KO) and wild type (WT) mice were examined by electroretinography (ERG), histology, RNA sequencing, and quantitative real-time PCR.

RESULTS

The amplitude of the photopic ERG elicited by the maximum stimulus intensity was smaller by 40% in the Ctrp9 KO mice than in WT mice at 8 weeks of age. However, the photopic ERGs was not reduced from 8 weeks to 6 months of age. The amplitudes of the scotopic ERGs were not reduced in the Ctrp9 KO mice at 8 weeks and 6 months of age. No distinct histological abnormalities were found in the retinal sections but the density of peanut agglutinin-stained cells in the retinal flat mount of KO mice was reduced to about 70% of that of WT mice. Genomewide RNA sequencing of the retina revealed the absence of the expression of CTRP9 in both KO and WT mice. RNA sequencing and quantitative real-time PCR analysis showed that the expressions of the transcripts of genes expressed in cones, Opn1sw, Opn1mw, Gnat2, and Cnga3, were reduced in the KO mice retina, however, the degree of expression of the transcripts in rods was not significantly reduced.

CONCLUSIONS

CTRP9 is released ectopically from other tissues, and it regulates the number of cones in the mouse retinas.

摘要

目的

C1q/TNF 相关蛋白(CTRP)9 是脂联素的同源物之一,其受体 AdipoR1 的基因缺失已知会导致视网膜变性。本研究的目的是确定 CTRP9 在视网膜中的作用。

方法

通过视网膜电图(ERG)、组织学、RNA 测序和定量实时 PCR 检查 Ctrp9 基因敲除(KO)和野生型(WT)小鼠的视网膜。

结果

在 8 周龄时,Ctrp9 KO 小鼠的最大刺激强度光诱发 ERG 的振幅比 WT 小鼠小 40%。然而,从 8 周龄到 6 个月龄,光诱发 ERG 没有降低。在 8 周龄和 6 个月龄时,Ctrp9 KO 小鼠的暗诱发 ERG 振幅没有降低。视网膜切片中未发现明显的组织学异常,但 KO 小鼠视网膜平片上花生凝集素染色细胞的密度降低至 WT 小鼠的约 70%。视网膜的全基因组 RNA 测序显示,KO 和 WT 小鼠中均不存在 CTRP9 的表达。RNA 测序和定量实时 PCR 分析显示,KO 小鼠视网膜中表达在视锥细胞中的基因的转录物的表达减少,Opn1sw、Opn1mw、Gnat2 和 Cnga3,但杆状细胞的转录物的表达程度没有明显降低。

结论

CTRP9 从其他组织异位释放,并调节小鼠视网膜中视锥细胞的数量。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b28a/9123514/2c530ebc3904/iovs-63-5-14-f006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b28a/9123514/a0e325767af3/iovs-63-5-14-f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b28a/9123514/40731d5be6c6/iovs-63-5-14-f002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b28a/9123514/8e20d13d6103/iovs-63-5-14-f003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b28a/9123514/2513d31525a6/iovs-63-5-14-f004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b28a/9123514/2d4651996d7b/iovs-63-5-14-f005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b28a/9123514/2c530ebc3904/iovs-63-5-14-f006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b28a/9123514/a0e325767af3/iovs-63-5-14-f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b28a/9123514/40731d5be6c6/iovs-63-5-14-f002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b28a/9123514/8e20d13d6103/iovs-63-5-14-f003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b28a/9123514/2513d31525a6/iovs-63-5-14-f004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b28a/9123514/2d4651996d7b/iovs-63-5-14-f005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b28a/9123514/2c530ebc3904/iovs-63-5-14-f006.jpg

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