MiR-18a-LncRNA NONRATG-022419 pairs targeted PRG-1 regulates diabetic induced cognitive impairment by regulating NGF\BDNF-Trkb signaling pathway.

IF 1.6 3区生物学 Q3 BIOCHEMICAL RESEARCH METHODS Proteome Science Pub Date : 2025-02-06 DOI:10.1186/s12953-025-00239-2

Qiong Xiang, Hu Lin, Jia-Sheng Tao, Chuan-Jun Fu, Li-Ni Liu, Jing Deng, Xian-Hui Li

{"title":"MiR-18a-LncRNA NONRATG-022419 pairs targeted PRG-1 regulates diabetic induced cognitive impairment by regulating NGF\\BDNF-Trkb signaling pathway.","authors":"Qiong Xiang, Hu Lin, Jia-Sheng Tao, Chuan-Jun Fu, Li-Ni Liu, Jing Deng, Xian-Hui Li","doi":"10.1186/s12953-025-00239-2","DOIUrl":null,"url":null,"abstract":"Background: Diabetic encephalopathy (DE) is considered as one of the complications of diabetes,which is associated with cognitive impairment in the pathological process of development. Up to now, phospholipid phosphatase related 4 (Plppr4), also known as plasticity related gene 1 (PRG-1) has been revealed its important role in neuroplasticity. However, the underlying mechanisms of Plppr4 on the basis of diabetic-induced cognitive dysfunction (DCD) are still unknown. The aim of current study was to provide insight into molecular mechanism and cellular heterogeneity underlying DCD, and investigate the functional role of PRG-1 involved in this process.Methods: Combined Single-cell RNA sequencing (scRNA-seq) and RNA transcriptome analysis, the distinct sub-populations, functional heterogeneity as well as potential enriched signaling pathways of hippocampal cells could be elucidated.Results: We identified the sub-cluster of type I spiral ganglion neurons expressed marker gene as Amigo2 in cluster8 and Cnr1 in cluster 9 of hippocampal cells from DCD and the effect of those on neuronal cells interaction. We also found that PRG-1 was involved in the synaptic plasticity regulation of hippocampus via NGF\\BDNF-Trkb signaling pathway. In high glucose induced HT22 cells injury model in vitro, we investigated that down-regulated PRG-1 along with down-regulated BDNF and also decreased expression of synapsin-1, PSD-95, SYN which are related to synaptic plasticity; Meanwhile, the Prg-1 targeted miR-18a-LncRNA NONRATG-022419 pairs related with significantly down-regulated expression of PRG-1.Conclusion: This study revealed the synaptic plasticity regulation of PRG-1 in DCD, and might provide the therapeutic target and potential biomarkers for early interventions in DCD patients.","PeriodicalId":20857,"journal":{"name":"Proteome Science","volume":"23 1","pages":"1"},"PeriodicalIF":1.6000,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11800523/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Proteome Science","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1186/s12953-025-00239-2","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"BIOCHEMICAL RESEARCH METHODS","Score":null,"Total":0}

引用次数: 0

Abstract

Background: Diabetic encephalopathy (DE) is considered as one of the complications of diabetes,which is associated with cognitive impairment in the pathological process of development. Up to now, phospholipid phosphatase related 4 (Plppr4), also known as plasticity related gene 1 (PRG-1) has been revealed its important role in neuroplasticity. However, the underlying mechanisms of Plppr4 on the basis of diabetic-induced cognitive dysfunction (DCD) are still unknown. The aim of current study was to provide insight into molecular mechanism and cellular heterogeneity underlying DCD, and investigate the functional role of PRG-1 involved in this process.

Methods: Combined Single-cell RNA sequencing (scRNA-seq) and RNA transcriptome analysis, the distinct sub-populations, functional heterogeneity as well as potential enriched signaling pathways of hippocampal cells could be elucidated.

Results: We identified the sub-cluster of type I spiral ganglion neurons expressed marker gene as Amigo2 in cluster8 and Cnr1 in cluster 9 of hippocampal cells from DCD and the effect of those on neuronal cells interaction. We also found that PRG-1 was involved in the synaptic plasticity regulation of hippocampus via NGF\BDNF-Trkb signaling pathway. In high glucose induced HT22 cells injury model in vitro, we investigated that down-regulated PRG-1 along with down-regulated BDNF and also decreased expression of synapsin-1, PSD-95, SYN which are related to synaptic plasticity; Meanwhile, the Prg-1 targeted miR-18a-LncRNA NONRATG-022419 pairs related with significantly down-regulated expression of PRG-1.

Conclusion: This study revealed the synaptic plasticity regulation of PRG-1 in DCD, and might provide the therapeutic target and potential biomarkers for early interventions in DCD patients.

Abstract Image

查看原文

微信好友朋友圈 QQ好友复制链接

本刊更多论文

MiR-18a-LncRNA NONRATG-022419对靶向PRG-1通过调节NGF\BDNF-Trkb信号通路调控糖尿病诱导的认知功能障碍。

背景：糖尿病性脑病（Diabetic encephalopathy， DE）被认为是糖尿病的并发症之一，在病理发展过程中伴有认知功能障碍。目前，磷脂磷酸酶相关基因4 （Plppr4）又称可塑性相关基因1 （PRG-1）在神经可塑性中的重要作用已被揭示。然而，Plppr4在糖尿病诱导的认知功能障碍（DCD）基础上的潜在机制尚不清楚。本研究旨在揭示DCD的分子机制和细胞异质性，并探讨PRG-1在这一过程中的功能作用。方法：结合单细胞RNA测序（scRNA-seq）和RNA转录组分析，阐明海马细胞的不同亚群、功能异质性和潜在的富集信号通路。结果：我们鉴定了DCD海马细胞第8簇表达标记基因Amigo2和第9簇表达标记基因Cnr1的I型螺旋神经节神经元亚簇及其对神经元相互作用的影响。我们还发现PRG-1通过NGF\BDNF-Trkb信号通路参与海马突触可塑性调节。在体外高糖诱导HT22细胞损伤模型中，我们研究了PRG-1的下调和BDNF的下调，以及与突触可塑性相关的突触素-1、PSD-95、SYN的表达降低；同时，Prg-1靶向的miR-18a-LncRNA NONRATG-022419对与Prg-1显著下调表达相关。结论：本研究揭示了PRG-1在DCD中突触可塑性的调控作用，可能为DCD患者早期干预提供治疗靶点和潜在的生物标志物。

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分钟内获得全文去求助

来源期刊

Proteome Science 生物-生化研究方法

CiteScore

2.90

自引率

0.00%

发文量

审稿时长

4.5 months

期刊介绍： Proteome Science is an open access journal publishing research in the area of systems studies. Proteome Science considers manuscripts based on all aspects of functional and structural proteomics, genomics, metabolomics, systems analysis and metabiome analysis. It encourages the submissions of studies that use large-scale or systems analysis of biomolecules in a cellular, organismal and/or environmental context. Studies that describe novel biological or clinical insights as well as methods-focused studies that describe novel methods for the large-scale study of any and all biomolecules in cells and tissues, such as mass spectrometry, protein and nucleic acid microarrays, genomics, next-generation sequencing and computational algorithms and methods are all within the scope of Proteome Science, as are electron topography, structural methods, proteogenomics, chemical proteomics, stem cell proteomics, organelle proteomics, plant and microbial proteomics. In spite of its name, Proteome Science considers all aspects of large-scale and systems studies because ultimately any mechanism that results in genomic and metabolomic changes will affect or be affected by the proteome. To reflect this intrinsic relationship of biological systems, Proteome Science will consider all such articles.