{"title":"LncRNA RP11-773H22.4 is upregulated in severe pneumonia and may be a diagnostic and prognostic marker for severe pneumonia.","authors":"Yan Cao, Feiyan Wang","doi":"10.1684/abc.2024.1886","DOIUrl":null,"url":null,"abstract":"<p><p>The incidence of pneumonia has become increasingly prevalent, and its severity has been continuously escalating, bringing significant damage and stress to people's lives. The regulatory role of RP11-773H22.4 in the onset and development of severe pneumonia is emerging as an important factor, however, the exact mechanisms controlling its effects have not been fully elucidated. ROC curve and Kaplan-Meier curve were employed to assess the diagnostic and prognostic significance of RP11-773H22.4 in severe pneumonia. qRT-PCR was employed to assess the RP11-773H22.4 and miR-1287-5p expression. The CCK-8 was employed to assess cell viability. The rate of apoptosis was measured utilizing flow cytometric. The concentration of inflammatory factors was detected by ELISA kit. The interaction between RP11-773H22.4 and miR-1287-5p was verified by dual luciferase reporter gene assay. In individuals afflicted with severe pneumonia, there was an observed up-regulation in RP11-773H22.4 expression and a corresponding decline in miR-1287-5p expression. RP11-773H22.4 demonstrated diagnostic and prognostic significance for severe pneumonia. RP11-773H22.4 augmented the viability of MRC-5 cells with LPS treatment by modulating miR-1287-5p, leading to a reduction in apoptosis and lower levels of inflammatory cytokines. RP11-773H22.4 was highly expressed in severe pneumonia and may serve as a diagnostic and prognostic marker for severe pneumonia. miR-1287-5p was downregulated in severe pneumonia, and RP11-773H22.4 participated in the pathogenesis of severe pneumonia by regulating the expression of miR-1287-5p.</p>","PeriodicalId":93870,"journal":{"name":"Annales de biologie clinique","volume":"82 2","pages":"187-199"},"PeriodicalIF":0.0000,"publicationDate":"2024-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Annales de biologie clinique","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1684/abc.2024.1886","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
The incidence of pneumonia has become increasingly prevalent, and its severity has been continuously escalating, bringing significant damage and stress to people's lives. The regulatory role of RP11-773H22.4 in the onset and development of severe pneumonia is emerging as an important factor, however, the exact mechanisms controlling its effects have not been fully elucidated. ROC curve and Kaplan-Meier curve were employed to assess the diagnostic and prognostic significance of RP11-773H22.4 in severe pneumonia. qRT-PCR was employed to assess the RP11-773H22.4 and miR-1287-5p expression. The CCK-8 was employed to assess cell viability. The rate of apoptosis was measured utilizing flow cytometric. The concentration of inflammatory factors was detected by ELISA kit. The interaction between RP11-773H22.4 and miR-1287-5p was verified by dual luciferase reporter gene assay. In individuals afflicted with severe pneumonia, there was an observed up-regulation in RP11-773H22.4 expression and a corresponding decline in miR-1287-5p expression. RP11-773H22.4 demonstrated diagnostic and prognostic significance for severe pneumonia. RP11-773H22.4 augmented the viability of MRC-5 cells with LPS treatment by modulating miR-1287-5p, leading to a reduction in apoptosis and lower levels of inflammatory cytokines. RP11-773H22.4 was highly expressed in severe pneumonia and may serve as a diagnostic and prognostic marker for severe pneumonia. miR-1287-5p was downregulated in severe pneumonia, and RP11-773H22.4 participated in the pathogenesis of severe pneumonia by regulating the expression of miR-1287-5p.