tRNA-derived fragment tRF-30 propels diabetes-induced retinal microvascular complications by regulating STAT3 signaling

IF 3.3 3区生物学 Q3 CELL BIOLOGY

Cell Biology International Pub Date : 2024-07-12 DOI:10.1002/cbin.12210

Dongqing Yuan, Yingnan Xu, Lian Xue, Weiwei Zhang, Liuwei Gu, Qinghuai Liu

{"title":"tRNA-derived fragment tRF-30 propels diabetes-induced retinal microvascular complications by regulating STAT3 signaling","authors":"Dongqing Yuan, Yingnan Xu, Lian Xue, Weiwei Zhang, Liuwei Gu, Qinghuai Liu","doi":"10.1002/cbin.12210","DOIUrl":null,"url":null,"abstract":"<p>Transfer RNA-derived fragments (tRFs) represent a novel class of non-coding RNA transcripts that possess specific biological functions. However, the involvement of tRFs in retinal microvascular diseases remains poorly understood. In this study, we aimed to reveal whether modulation of tRF-30 expression could attenuate pathological retinal neovascular diseases. Our findings demonstrate a significant upregulation of tRF-30 expression levels in both in vivo models of diabetic retinopathy (DR) and in vitro endothelial sprouting models. Conversely, inhibition of tRF-30 expression suppressed the formation of abnormal neovascularization in the retina in vivo, while reducing the proliferation and migration activity of retinal vascular endothelial cells in vitro. We also found that tRF-30 modulates retinal neovascularization through the tRF-30/TRIB3/signal transducer and activated transcription 3 signaling pathway. Furthermore, we validated a significant upregulation of tRF-30 expression levels in the vitreous humor of DR patients, with high levels of both validity and specificity in diagnostic testing. Collectively, our findings highlight a pro-angiogenic role for tRF-30 in DR. Intervening in the tRF-30 signaling pathway may represent a promising prevention and treatment strategy for retinal angiogenesis.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"48 10","pages":"1548-1558"},"PeriodicalIF":3.3000,"publicationDate":"2024-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cell Biology International","FirstCategoryId":"99","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/cbin.12210","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"CELL BIOLOGY","Score":null,"Total":0}

引用次数: 0

Abstract

Transfer RNA-derived fragments (tRFs) represent a novel class of non-coding RNA transcripts that possess specific biological functions. However, the involvement of tRFs in retinal microvascular diseases remains poorly understood. In this study, we aimed to reveal whether modulation of tRF-30 expression could attenuate pathological retinal neovascular diseases. Our findings demonstrate a significant upregulation of tRF-30 expression levels in both in vivo models of diabetic retinopathy (DR) and in vitro endothelial sprouting models. Conversely, inhibition of tRF-30 expression suppressed the formation of abnormal neovascularization in the retina in vivo, while reducing the proliferation and migration activity of retinal vascular endothelial cells in vitro. We also found that tRF-30 modulates retinal neovascularization through the tRF-30/TRIB3/signal transducer and activated transcription 3 signaling pathway. Furthermore, we validated a significant upregulation of tRF-30 expression levels in the vitreous humor of DR patients, with high levels of both validity and specificity in diagnostic testing. Collectively, our findings highlight a pro-angiogenic role for tRF-30 in DR. Intervening in the tRF-30 signaling pathway may represent a promising prevention and treatment strategy for retinal angiogenesis.

查看原文本刊更多论文

tRNA衍生片段tRF-30通过调节STAT3信号传导推动糖尿病诱发的视网膜微血管并发症。

转运核糖核酸衍生片段（tRFs）是一类新型的非编码核糖核酸转录本，具有特定的生物学功能。然而，人们对 tRFs 参与视网膜微血管疾病的情况仍知之甚少。在这项研究中，我们旨在揭示调节 tRF-30 的表达能否减轻病理性视网膜新生血管疾病。我们的研究结果表明，在体内糖尿病视网膜病变（DR）模型和体外内皮萌芽模型中，tRF-30 的表达水平都有明显上调。相反，抑制 tRF-30 的表达可抑制体内视网膜异常新生血管的形成，同时降低体外视网膜血管内皮细胞的增殖和迁移活性。我们还发现，tRF-30 通过 tRF-30/TRIB3/signal transducer and activated transcription 3 信号转导途径调节视网膜新生血管的形成。此外，我们还验证了 DR 患者玻璃体中 tRF-30 表达水平的显著上调，在诊断测试中具有高度的有效性和特异性。总之，我们的研究结果凸显了 tRF-30 在 DR 中的促血管生成作用。干预 tRF-30 信号通路可能是一种很有前景的视网膜血管生成预防和治疗策略。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Cell Biology International 生物-细胞生物学

CiteScore

7.60

自引率

0.00%

发文量

208

审稿时长

1 months

期刊介绍： Each month, the journal publishes easy-to-assimilate, up-to-the minute reports of experimental findings by researchers using a wide range of the latest techniques. Promoting the aims of cell biologists worldwide, papers reporting on structure and function - especially where they relate to the physiology of the whole cell - are strongly encouraged. Molecular biology is welcome, as long as articles report findings that are seen in the wider context of cell biology. In covering all areas of the cell, the journal is both appealing and accessible to a broad audience. Authors whose papers do not appeal to cell biologists in general because their topic is too specialized (e.g. infectious microbes, protozoology) are recommended to send them to more relevant journals. Papers reporting whole animal studies or work more suited to a medical journal, e.g. histopathological studies or clinical immunology, are unlikely to be accepted, unless they are fully focused on some important cellular aspect. These last remarks extend particularly to papers on cancer. Unless firmly based on some deeper cellular or molecular biological principle, papers that are highly specialized in this field, with limited appeal to cell biologists at large, should be directed towards journals devoted to cancer, there being very many from which to choose.