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蛋白质组学鉴定出多种与 Pde6b 突变小鼠模型中视网膜变性相关的视网膜色素变性相关蛋白。

Proteomics identifies multiple retinitis pigmentosa associated proteins involved in retinal degeneration in a mouse model bearing a Pde6b mutation.

机构信息

Henan Provincial People's Hospital, Henan Eye Hospital, People's Hospital of Zhengzhou University, Zhengzhou, Henan, 450003, China.

Eye Institute, Henan Academy of Innovations in Medical Science, Zhengzhou, Henan, 450003, China.

出版信息

Sci Rep. 2024 Sep 27;14(1):22090. doi: 10.1038/s41598-024-72821-1.

Abstract

Retinitis pigmentosa (RP) is a progressive and degenerative retinal disease resulting in severe vision loss. RP have been extensively studied for pathogenetic mechanisms and treatments. Yet there is little information about alterations of RP associated proteins in phosphodiesterase 6 beta (Pde6b) mutated model. To explore the roles of RP causing proteins, we performed a label free quantitative mass spectrometry based proteomic analysis in rd10 mouse retinas. 3737 proteins were identified at the degenerative time points in rd10 mice. 222 and 289 differentially expressed proteins (DEPs) (fold change, FC > 2, p < 0.05) were detected at 5 and 8 weeks. Based on Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses, visual perception and phototransduction were severely affected. The downregulated DEPs were significantly enriched in cilium assembly and protein localization. 25 decreased DEPs causing autosomal recessive/dominant retinitis pigmentosa were visualized by heatmaps. Protein-protein interaction network represented 13 DEPs interacted directly with Pde6b protein. 25 DEPs causing RP were involved in phototransduction, visual perception, response to stimulus, protein localization and cilium assembly pathways. The significantly reduced expressions of DEPs were further validated by quantitative reverse transcription polymerase chain reaction (qPCR), Western blots (WB) and immunohistochemistry (IHC). This study revealed the molecular mechanisms underlying early and late stage of RP, as well as changes of RP-causing proteins.

摘要

色素性视网膜炎(RP)是一种进行性和退行性视网膜疾病,导致严重的视力丧失。已经对 RP 的发病机制和治疗进行了广泛的研究。然而,关于磷酸二酯酶 6β(Pde6b)突变模型中与 RP 相关的蛋白改变的信息很少。为了探讨致 RP 蛋白的作用,我们在 rd10 小鼠视网膜中进行了无标记定量质谱蛋白质组学分析。在 rd10 小鼠的退行性时间点鉴定出 3737 种蛋白质。在 5 周和 8 周时检测到 222 和 289 种差异表达蛋白(DEPs)(倍数变化,FC>2,p<0.05)。基于基因本体论(GO)和京都基因与基因组百科全书(KEGG)途径分析,视觉感知和光转导受到严重影响。下调的 DEPs 在纤毛组装和蛋白质定位中显著富集。通过热图可视化了 25 种导致常染色体隐性/显性色素性视网膜炎的下调 DEPs。蛋白质-蛋白质相互作用网络代表 13 个 DEP 与 Pde6b 蛋白直接相互作用。25 种致 RP 的 DEP 参与光转导、视觉感知、对刺激的反应、蛋白质定位和纤毛组装途径。通过定量逆转录聚合酶链反应(qPCR)、Western blot(WB)和免疫组织化学(IHC)进一步验证了 DEP 的显著低表达。该研究揭示了 RP 早期和晚期的分子机制,以及 RP 致病蛋白的变化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9dbf/11437026/f370334e93a8/41598_2024_72821_Fig1_HTML.jpg

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