{"title":"Exploring the Regulatory Interaction of Differentially Expressed Proteins in Cleft Palate Induced by Retinoic Acid.","authors":"Liyun Chen, Aiwei Ma, Lewen Jiang, Jufeng Fan, Wenshi Jiang, Mengjing Xu, Xujue Bai, Jianda Zhou, Wancong Zhang, Shijie Tang","doi":"10.2174/0109298665308502240820115618","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to identify novel proteins involved in retinoic acid (RA)-induced embryonic cleft palate development.</p><p><strong>Method: </strong>The palate tissues of the control and RA-treated E14.5 were dissected and subjected to iTRAQ-based proteomic analysis.</p><p><strong>Results: </strong>Differential expression analysis identified 196 significantly upregulated and 149 downregulated considerably proteins in RA-induced palate tissues. Comprehensive Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analysis revealed the significant involvement of cytoplasmic translation, ribosome biogenesis, glycolysis/gluconeogenesis, and glutathione metabolism pathways in cleft palate pathogenesis triggered by RA. In particular, ribosome-related pathways were highly enriched, while glycolysis was disrupted. Protein-protein interaction analysis, facilitated by the STRING database, revealed a tightly interconnected network of differentially expressed proteins. Further analysis using the cytoHubba plugin in Cytoscape identified ten hub proteins, including Eif4a1, Gapdh, Eno1, Imp3, Rps20, Rps27a, Eef2, Hsp90ab1, Rpl19, and Rps16, indicating their potential roles in RA-induced cleft palate development, and thus positioning them as potential biomarkers for cleft palate.</p><p><strong>Conclusion: </strong>These findings provide valuable insights into the proteomic changes associated with RA-induced cleft palate and shed light on key pathways and proteins that can contribute significantly to the pathogenesis of this congenital condition.</p>","PeriodicalId":20736,"journal":{"name":"Protein and Peptide Letters","volume":" ","pages":""},"PeriodicalIF":1.0000,"publicationDate":"2024-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Protein and Peptide Letters","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.2174/0109298665308502240820115618","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Objective: This study aimed to identify novel proteins involved in retinoic acid (RA)-induced embryonic cleft palate development.
Method: The palate tissues of the control and RA-treated E14.5 were dissected and subjected to iTRAQ-based proteomic analysis.
Results: Differential expression analysis identified 196 significantly upregulated and 149 downregulated considerably proteins in RA-induced palate tissues. Comprehensive Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analysis revealed the significant involvement of cytoplasmic translation, ribosome biogenesis, glycolysis/gluconeogenesis, and glutathione metabolism pathways in cleft palate pathogenesis triggered by RA. In particular, ribosome-related pathways were highly enriched, while glycolysis was disrupted. Protein-protein interaction analysis, facilitated by the STRING database, revealed a tightly interconnected network of differentially expressed proteins. Further analysis using the cytoHubba plugin in Cytoscape identified ten hub proteins, including Eif4a1, Gapdh, Eno1, Imp3, Rps20, Rps27a, Eef2, Hsp90ab1, Rpl19, and Rps16, indicating their potential roles in RA-induced cleft palate development, and thus positioning them as potential biomarkers for cleft palate.
Conclusion: These findings provide valuable insights into the proteomic changes associated with RA-induced cleft palate and shed light on key pathways and proteins that can contribute significantly to the pathogenesis of this congenital condition.
目的：本研究旨在鉴定参与视黄酸（RA）诱导胚胎腭裂发育的新型蛋白质：本研究旨在鉴定参与视黄酸（RA）诱导的胚胎腭裂发育的新型蛋白质：方法：解剖E14.5对照组和RA处理组的腭裂组织，并进行基于iTRAQ的蛋白质组分析：结果：差异表达分析在RA诱导的腭组织中发现了196个明显上调的蛋白和149个明显下调的蛋白。基因本体和京都基因组百科全书的综合富集分析表明，细胞质翻译、核糖体生物发生、糖酵解/糖原生成和谷胱甘肽代谢途径在 RA 引发的腭裂发病机制中有重要参与。其中，核糖体相关通路高度富集，而糖酵解则受到破坏。利用 STRING 数据库进行的蛋白质-蛋白质相互作用分析揭示了一个紧密相连的差异表达蛋白质网络。利用Cytoscape中的cytoHubba插件进行的进一步分析发现了10个枢纽蛋白，包括Eif4a1、Gapdh、Eno1、Imp3、Rps20、Rps27a、Eef2、Hsp90ab1、Rpl19和Rps16，这表明它们在RA诱导的腭裂发育过程中可能发挥作用，从而将它们定位为腭裂的潜在生物标记物：这些发现为了解与 RA 诱导的腭裂相关的蛋白质组变化提供了宝贵的信息，并揭示了可能对这种先天性疾病的发病机制有重大影响的关键通路和蛋白质。
期刊介绍：
Protein & Peptide Letters publishes letters, original research papers, mini-reviews and guest edited issues in all important aspects of protein and peptide research, including structural studies, advances in recombinant expression, function, synthesis, enzymology, immunology, molecular modeling, and drug design. Manuscripts must have a significant element of novelty, timeliness and urgency that merit rapid publication. Reports of crystallization and preliminary structure determination of biologically important proteins are considered only if they include significant new approaches or deal with proteins of immediate importance, and preliminary structure determinations of biologically important proteins. Purely theoretical/review papers should provide new insight into the principles of protein/peptide structure and function. Manuscripts describing computational work should include some experimental data to provide confirmation of the results of calculations.
Protein & Peptide Letters focuses on:
Structure Studies
Advances in Recombinant Expression
Drug Design
Chemical Synthesis
Function
Pharmacology
Enzymology
Conformational Analysis
Immunology
Biotechnology
Protein Engineering
Protein Folding
Sequencing
Molecular Recognition
Purification and Analysis
京公网安备 11010802042870号
京ICP备2023020795号-1
分享
求助内容：
应助结果提醒方式：
扫码关注我们
