Zengli Yu , Yaxin Zhang , Guoxu Wang , Shuaixing Song , Hexin Su , Yang Wu , Yuwei Zhang , Pengfei Liu , Xiaozhuan Liu
{"title":"全反式维甲酸诱发腭裂的机制可能与新型ENSMUST00000159153-miR-137-5p-Wnt7a和ENSMUST000000236086-miR-34b-3p-EphA10/TRPM2 ceRNA串扰有关。","authors":"Zengli Yu , Yaxin Zhang , Guoxu Wang , Shuaixing Song , Hexin Su , Yang Wu , Yuwei Zhang , Pengfei Liu , Xiaozhuan Liu","doi":"10.1016/j.etap.2024.104623","DOIUrl":null,"url":null,"abstract":"<div><div>Cleft palate is the most prevalent congenital condition. Cleft palate is brought on by an exogenous chemical called all-trans retinoic acid (atRA). In order to indirectly control gene expression, long chain non-coding RNAs (lncRNAs) act as competitive endogenous RNA (ceRNA) sponges. Its exact mode of action in cleft palate has not yet been determined. The purpose of this study was to determine whether lncRNAs and miRNAs regulated palatal fusion genes during the formation of cleft palate and to offer a possible course for cleft palate target gene therapy. In this work, we created a cleft palate model using atRA, conducted RNA sequencing (RNA-seq) to identify the genes that differed between the atRA-treated group and the control group, and built the lncRNA-miRNA-mRNA ceRNA network based on the projected ceRNA. The results were confirmed using a quantitative real-time polymerase chain reaction (qRT-PCR). ENSMUST00000159153-miR-137–5p-Wnt7a and ENSMUST000000236086-miR-34b-3p-EphA10/TRPM2 may be the main causes of atRA-induced cleft palate, according to the results.</div></div>","PeriodicalId":11775,"journal":{"name":"Environmental toxicology and pharmacology","volume":"114 ","pages":"Article 104623"},"PeriodicalIF":4.2000,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"The mechanism of all-trans retinoic acid-induced cleft palate may be related to the novel ENSMUST00000159153-miR-137–5p-Wnt7a and ENSMUST000000236086-miR-34b-3p-EphA10/TRPM2 ceRNA crosstalk\",\"authors\":\"Zengli Yu , Yaxin Zhang , Guoxu Wang , Shuaixing Song , Hexin Su , Yang Wu , Yuwei Zhang , Pengfei Liu , Xiaozhuan Liu\",\"doi\":\"10.1016/j.etap.2024.104623\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>Cleft palate is the most prevalent congenital condition. Cleft palate is brought on by an exogenous chemical called all-trans retinoic acid (atRA). In order to indirectly control gene expression, long chain non-coding RNAs (lncRNAs) act as competitive endogenous RNA (ceRNA) sponges. Its exact mode of action in cleft palate has not yet been determined. The purpose of this study was to determine whether lncRNAs and miRNAs regulated palatal fusion genes during the formation of cleft palate and to offer a possible course for cleft palate target gene therapy. In this work, we created a cleft palate model using atRA, conducted RNA sequencing (RNA-seq) to identify the genes that differed between the atRA-treated group and the control group, and built the lncRNA-miRNA-mRNA ceRNA network based on the projected ceRNA. The results were confirmed using a quantitative real-time polymerase chain reaction (qRT-PCR). ENSMUST00000159153-miR-137–5p-Wnt7a and ENSMUST000000236086-miR-34b-3p-EphA10/TRPM2 may be the main causes of atRA-induced cleft palate, according to the results.</div></div>\",\"PeriodicalId\":11775,\"journal\":{\"name\":\"Environmental toxicology and pharmacology\",\"volume\":\"114 \",\"pages\":\"Article 104623\"},\"PeriodicalIF\":4.2000,\"publicationDate\":\"2024-12-20\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Environmental toxicology and pharmacology\",\"FirstCategoryId\":\"93\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S1382668924002631\",\"RegionNum\":3,\"RegionCategory\":\"环境科学与生态学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"ENVIRONMENTAL SCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Environmental toxicology and pharmacology","FirstCategoryId":"93","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1382668924002631","RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"ENVIRONMENTAL SCIENCES","Score":null,"Total":0}
The mechanism of all-trans retinoic acid-induced cleft palate may be related to the novel ENSMUST00000159153-miR-137–5p-Wnt7a and ENSMUST000000236086-miR-34b-3p-EphA10/TRPM2 ceRNA crosstalk
Cleft palate is the most prevalent congenital condition. Cleft palate is brought on by an exogenous chemical called all-trans retinoic acid (atRA). In order to indirectly control gene expression, long chain non-coding RNAs (lncRNAs) act as competitive endogenous RNA (ceRNA) sponges. Its exact mode of action in cleft palate has not yet been determined. The purpose of this study was to determine whether lncRNAs and miRNAs regulated palatal fusion genes during the formation of cleft palate and to offer a possible course for cleft palate target gene therapy. In this work, we created a cleft palate model using atRA, conducted RNA sequencing (RNA-seq) to identify the genes that differed between the atRA-treated group and the control group, and built the lncRNA-miRNA-mRNA ceRNA network based on the projected ceRNA. The results were confirmed using a quantitative real-time polymerase chain reaction (qRT-PCR). ENSMUST00000159153-miR-137–5p-Wnt7a and ENSMUST000000236086-miR-34b-3p-EphA10/TRPM2 may be the main causes of atRA-induced cleft palate, according to the results.
期刊介绍:
Environmental Toxicology and Pharmacology publishes the results of studies concerning toxic and pharmacological effects of (human and veterinary) drugs and of environmental contaminants in animals and man.
Areas of special interest are: molecular mechanisms of toxicity, biotransformation and toxicokinetics (including toxicokinetic modelling), molecular, biochemical and physiological mechanisms explaining differences in sensitivity between species and individuals, the characterisation of pathophysiological models and mechanisms involved in the development of effects and the identification of biological markers that can be used to study exposure and effects in man and animals.
In addition to full length papers, short communications, full-length reviews and mini-reviews, Environmental Toxicology and Pharmacology will publish in depth assessments of special problem areas. The latter publications may exceed the length of a full length paper three to fourfold. A basic requirement is that the assessments are made under the auspices of international groups of leading experts in the fields concerned. The information examined may either consist of data that were already published, or of new data that were obtained within the framework of collaborative research programmes. Provision is also made for the acceptance of minireviews on (classes of) compounds, toxicities or mechanisms, debating recent advances in rapidly developing fields that fall within the scope of the journal.