{"title":"MicroRNA-34-5p调控蜱唾液腺变性过程中ECR的表达。","authors":"Shanming Hu, Yanan Wang, Yongzhi Zhou, Jie Cao, Houshuang Zhang, Jinlin Zhou","doi":"10.1186/s13071-025-06842-8","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>The salivary glands of female ticks rapidly degenerate after feeding via programmed cell death mediated by an ecdysteroid receptor (ECR). The degeneration includes both apoptosis and autophagy. The process of degeneration can also be regulated by microRNAs (miRNAs), but the underlying mechanism of miRNA involvement in salivary gland degeneration remains incompletely understood. Here, we demonstrate that microRNA34-5p (miR-34-5p) regulates the process of salivary gland degeneration in Rhipicephalus haemaphysaloides by modulating the target gene RhECR.</p><p><strong>Methods: </strong>Dual luciferase reporter assays and phenotypic rescue experiments identified RhECR as a direct target of miR-34-5p. The overexpression and inhibition of miR-34-5p were quantified by hematoxylin and eosin (H&E) and Terminal deoxynucleotidyl transferase dUTP Nick-End Labeling (TUNEL) staining.</p><p><strong>Results: </strong>The results showed that miR-34-5p inhibited the expression of RhECR to retard apoptosis in salivary gland acini. The study identified the roles of miR-34-5p and RhECR and their interactions in tick salivary gland degeneration.</p><p><strong>Conclusions: </strong>The findings will aid in the application of ECR genes for tick control.</p>","PeriodicalId":19793,"journal":{"name":"Parasites & Vectors","volume":"18 1","pages":"187"},"PeriodicalIF":3.0000,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12100847/pdf/","citationCount":"0","resultStr":"{\"title\":\"MicroRNA-34-5p regulates the expression of ecdysteroid receptor (ECR) in the process of salivary gland degeneration of ticks.\",\"authors\":\"Shanming Hu, Yanan Wang, Yongzhi Zhou, Jie Cao, Houshuang Zhang, Jinlin Zhou\",\"doi\":\"10.1186/s13071-025-06842-8\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>The salivary glands of female ticks rapidly degenerate after feeding via programmed cell death mediated by an ecdysteroid receptor (ECR). The degeneration includes both apoptosis and autophagy. The process of degeneration can also be regulated by microRNAs (miRNAs), but the underlying mechanism of miRNA involvement in salivary gland degeneration remains incompletely understood. Here, we demonstrate that microRNA34-5p (miR-34-5p) regulates the process of salivary gland degeneration in Rhipicephalus haemaphysaloides by modulating the target gene RhECR.</p><p><strong>Methods: </strong>Dual luciferase reporter assays and phenotypic rescue experiments identified RhECR as a direct target of miR-34-5p. The overexpression and inhibition of miR-34-5p were quantified by hematoxylin and eosin (H&E) and Terminal deoxynucleotidyl transferase dUTP Nick-End Labeling (TUNEL) staining.</p><p><strong>Results: </strong>The results showed that miR-34-5p inhibited the expression of RhECR to retard apoptosis in salivary gland acini. The study identified the roles of miR-34-5p and RhECR and their interactions in tick salivary gland degeneration.</p><p><strong>Conclusions: </strong>The findings will aid in the application of ECR genes for tick control.</p>\",\"PeriodicalId\":19793,\"journal\":{\"name\":\"Parasites & Vectors\",\"volume\":\"18 1\",\"pages\":\"187\"},\"PeriodicalIF\":3.0000,\"publicationDate\":\"2025-05-23\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12100847/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Parasites & Vectors\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1186/s13071-025-06842-8\",\"RegionNum\":2,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"PARASITOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Parasites & Vectors","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1186/s13071-025-06842-8","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"PARASITOLOGY","Score":null,"Total":0}
MicroRNA-34-5p regulates the expression of ecdysteroid receptor (ECR) in the process of salivary gland degeneration of ticks.
Background: The salivary glands of female ticks rapidly degenerate after feeding via programmed cell death mediated by an ecdysteroid receptor (ECR). The degeneration includes both apoptosis and autophagy. The process of degeneration can also be regulated by microRNAs (miRNAs), but the underlying mechanism of miRNA involvement in salivary gland degeneration remains incompletely understood. Here, we demonstrate that microRNA34-5p (miR-34-5p) regulates the process of salivary gland degeneration in Rhipicephalus haemaphysaloides by modulating the target gene RhECR.
Methods: Dual luciferase reporter assays and phenotypic rescue experiments identified RhECR as a direct target of miR-34-5p. The overexpression and inhibition of miR-34-5p were quantified by hematoxylin and eosin (H&E) and Terminal deoxynucleotidyl transferase dUTP Nick-End Labeling (TUNEL) staining.
Results: The results showed that miR-34-5p inhibited the expression of RhECR to retard apoptosis in salivary gland acini. The study identified the roles of miR-34-5p and RhECR and their interactions in tick salivary gland degeneration.
Conclusions: The findings will aid in the application of ECR genes for tick control.
期刊介绍：
Parasites & Vectors is an open access, peer-reviewed online journal dealing with the biology of parasites, parasitic diseases, intermediate hosts, vectors and vector-borne pathogens. Manuscripts published in this journal will be available to all worldwide, with no barriers to access, immediately following acceptance. However, authors retain the copyright of their material and may use it, or distribute it, as they wish.
Manuscripts on all aspects of the basic and applied biology of parasites, intermediate hosts, vectors and vector-borne pathogens will be considered. In addition to the traditional and well-established areas of science in these fields, we also aim to provide a vehicle for publication of the rapidly developing resources and technology in parasite, intermediate host and vector genomics and their impacts on biological research. We are able to publish large datasets and extensive results, frequently associated with genomic and post-genomic technologies, which are not readily accommodated in traditional journals. Manuscripts addressing broader issues, for example economics, social sciences and global climate change in relation to parasites, vectors and disease control, are also welcomed.
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