Feline hypertrophic cardiomyopathy: Does the microRNA-mRNA regulatory network contribute to heart sarcomeric protein remodelling?

IF 1.8 4区医学 Q3 PATHOLOGY International Journal of Experimental Pathology Pub Date : 2024-08-13 DOI:10.1111/iep.12514

Gabriella Guelfi, Noemi Venanzi, Camilla Capaccia, Valentina Stefanetti, Chiara Brachelente, Monica Sforna, Francesco Porciello, Elvio Lepri

{"title":"Feline hypertrophic cardiomyopathy: Does the microRNA-mRNA regulatory network contribute to heart sarcomeric protein remodelling?","authors":"Gabriella Guelfi, Noemi Venanzi, Camilla Capaccia, Valentina Stefanetti, Chiara Brachelente, Monica Sforna, Francesco Porciello, Elvio Lepri","doi":"10.1111/iep.12514","DOIUrl":null,"url":null,"abstract":"Feline primary hypertrophic cardiomyopathy (HCM) is an intrinsic myocardial disease characterized by concentric hypertrophy of the left ventricle. In the present study, we investigated the microRNA-mRNA regulatory network in feline myocardial tissue affected by primary (HCMI) and secondary HCM (HCMII). MRNA expression levels of sarcomeric genes, including, TNNT2, TNNI3, MYH7, MYBPC3, TPM1 and ACTC1 were assessed in the FFPE myocardial tissues. FFPE tissues from healthy cats were sequenced by the NGS, to explore, in the entire non-deposited miRNome, the expression level of microRNAs targeting the complementary sequences of selected sarcomeric mRNAs. The sarcomeric genes TNNT2, MYH7, MYBPC3 and TPM1 showed a statistically significant upregulation in HCMI compared to HCMII (p < .01), except ACTC1 which was downregulated (p < .01); TNNI3 showed no statistically significant difference. In HCMII miR-122-5p, miR-338-3p, miR-484, miR-370-3p, miR-92b-3p, miR-375 and miR-370-3p showed a significant upregulation (p < .01) compared to control. The exception was miR-30a-5p which showed downregulation. Worthy of note is the 4-fold higher expression of miR-370-3p, a key regulator of MYBPC3, in HMCI compared to HMCII. This research does not solve the aetiological mystery of HCM, but it may help to find a way to help diagnose and define the prognosis of HCM in cats.","PeriodicalId":14157,"journal":{"name":"International Journal of Experimental Pathology","volume":"105 5","pages":"170-183"},"PeriodicalIF":1.8000,"publicationDate":"2024-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/iep.12514","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"International Journal of Experimental Pathology","FirstCategoryId":"3","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1111/iep.12514","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"PATHOLOGY","Score":null,"Total":0}

引用次数: 0

Abstract

Feline primary hypertrophic cardiomyopathy (HCM) is an intrinsic myocardial disease characterized by concentric hypertrophy of the left ventricle. In the present study, we investigated the microRNA-mRNA regulatory network in feline myocardial tissue affected by primary (HCMI) and secondary HCM (HCMII). MRNA expression levels of sarcomeric genes, including, TNNT2, TNNI3, MYH7, MYBPC3, TPM1 and ACTC1 were assessed in the FFPE myocardial tissues. FFPE tissues from healthy cats were sequenced by the NGS, to explore, in the entire non-deposited miRNome, the expression level of microRNAs targeting the complementary sequences of selected sarcomeric mRNAs. The sarcomeric genes TNNT2, MYH7, MYBPC3 and TPM1 showed a statistically significant upregulation in HCMI compared to HCMII (p < .01), except ACTC1 which was downregulated (p < .01); TNNI3 showed no statistically significant difference. In HCMII miR-122-5p, miR-338-3p, miR-484, miR-370-3p, miR-92b-3p, miR-375 and miR-370-3p showed a significant upregulation (p < .01) compared to control. The exception was miR-30a-5p which showed downregulation. Worthy of note is the 4-fold higher expression of miR-370-3p, a key regulator of MYBPC3, in HMCI compared to HMCII. This research does not solve the aetiological mystery of HCM, but it may help to find a way to help diagnose and define the prognosis of HCM in cats.

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

猫肥厚性心肌病：微RNA-mRNA调控网络是否有助于心脏肉瘤蛋白重塑？

猫原发性肥厚性心肌病（HCM）是一种以左心室同心性肥厚为特征的内在心肌病。在本研究中，我们调查了受原发性（HCMI）和继发性（HCMII）肥厚性心肌病影响的猫心肌组织中的 microRNA-mRNA 调控网络。我们评估了 FFPE 心肌组织中肉瘤基因（包括 TNNT2、TNNI3、MYH7、MYBPC3、TPM1 和 ACTC1）的 MRNA 表达水平。对健康猫的 FFPE 组织进行了 NGS 测序，以探究在整个未沉积的 miRNome 中，以选定的肉瘤 mRNA 的互补序列为靶点的 microRNA 的表达水平。与 HCMII 相比，肉瘤基因 TNNT2、MYH7、MYBPC3 和 TPM1 在 HCMI 中的上调具有统计学意义（p＜0.05）。

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

International Journal of Experimental Pathology 医学-病理学

CiteScore

4.50

自引率

3.30%

发文量

审稿时长

>12 weeks

期刊介绍： Experimental Pathology encompasses the use of multidisciplinary scientific techniques to investigate the pathogenesis and progression of pathologic processes. The International Journal of Experimental Pathology - IJEP - publishes papers which afford new and imaginative insights into the basic mechanisms underlying human disease, including in vitro work, animal models, and clinical research. Aiming to report on work that addresses the common theme of mechanism at a cellular and molecular level, IJEP publishes both original experimental investigations and review articles. Recent themes for review series have covered topics as diverse as "Viruses and Cancer", "Granulomatous Diseases", "Stem cells" and "Cardiovascular Pathology".