Chuanrui Zhu, Lun Zhang, Hongfen Ma, Cuicui Zhang, Fang Cheng, Hong An, Wenxiang Zhu
{"title":"miR-193a-5p在新生儿急性呼吸窘迫综合征中的临床诊断价值及其对人肺上皮细胞的影响分析","authors":"Chuanrui Zhu, Lun Zhang, Hongfen Ma, Cuicui Zhang, Fang Cheng, Hong An, Wenxiang Zhu","doi":"10.1080/15513815.2024.2447579","DOIUrl":null,"url":null,"abstract":"<p><p><b>Aim</b>: To explore the clinical value of miR-193a-5p in neonatal acute respiratory distress syndrome (ARDS) and its role in ARDS cell model <i>in vitro</i>. <b>Methods</b>: RT-qPCR was utilized to detect miR-193a-5p level. Correlation analysis was implemented to assess the correlation between miR-193a-5p and clinical indicators (IL-6, IL-1β, TNF-α, LUS). Human lung epithelial cells induced by LPS were used to construct ARDS cell model. The effects of miR-193a-5p on cell viability, apoptosis and inflammation were evaluated by CCK-8, flow cytometry and ELISA. The target gene of miR-193a-5p was predicted and verified by StarBaseV2.0 and luciferase reporter gene, respectively. <b>Results</b>: MiR-193a-5p level in the ARDS group was down-regulated. MiR-193a-5p levels were negatively correlated with clinical indicators. <i>In vitro</i> studies revealed that up-regulation of miR-193a-5p significantly improved LPS-induced apoptosis, inflammation and viability inhibition. <b>Conclusion</b>: The expression of miR-193a-5p was decreased in neonatal ARDS, it is negatively correlated with the pro-inflammatory factors levels.</p>","PeriodicalId":50452,"journal":{"name":"Fetal and Pediatric Pathology","volume":" ","pages":"85-97"},"PeriodicalIF":0.7000,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Clinical Diagnostic Value of miR-193a-5p in Neonatal Acute Respiratory Distress Syndrome and Analysis of Its Effect on Human Lung Epithelial Cells.\",\"authors\":\"Chuanrui Zhu, Lun Zhang, Hongfen Ma, Cuicui Zhang, Fang Cheng, Hong An, Wenxiang Zhu\",\"doi\":\"10.1080/15513815.2024.2447579\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p><b>Aim</b>: To explore the clinical value of miR-193a-5p in neonatal acute respiratory distress syndrome (ARDS) and its role in ARDS cell model <i>in vitro</i>. <b>Methods</b>: RT-qPCR was utilized to detect miR-193a-5p level. Correlation analysis was implemented to assess the correlation between miR-193a-5p and clinical indicators (IL-6, IL-1β, TNF-α, LUS). Human lung epithelial cells induced by LPS were used to construct ARDS cell model. The effects of miR-193a-5p on cell viability, apoptosis and inflammation were evaluated by CCK-8, flow cytometry and ELISA. The target gene of miR-193a-5p was predicted and verified by StarBaseV2.0 and luciferase reporter gene, respectively. <b>Results</b>: MiR-193a-5p level in the ARDS group was down-regulated. MiR-193a-5p levels were negatively correlated with clinical indicators. <i>In vitro</i> studies revealed that up-regulation of miR-193a-5p significantly improved LPS-induced apoptosis, inflammation and viability inhibition. <b>Conclusion</b>: The expression of miR-193a-5p was decreased in neonatal ARDS, it is negatively correlated with the pro-inflammatory factors levels.</p>\",\"PeriodicalId\":50452,\"journal\":{\"name\":\"Fetal and Pediatric Pathology\",\"volume\":\" \",\"pages\":\"85-97\"},\"PeriodicalIF\":0.7000,\"publicationDate\":\"2025-03-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Fetal and Pediatric Pathology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1080/15513815.2024.2447579\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/1/23 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q4\",\"JCRName\":\"PATHOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Fetal and Pediatric Pathology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/15513815.2024.2447579","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/23 0:00:00","PubModel":"Epub","JCR":"Q4","JCRName":"PATHOLOGY","Score":null,"Total":0}
Clinical Diagnostic Value of miR-193a-5p in Neonatal Acute Respiratory Distress Syndrome and Analysis of Its Effect on Human Lung Epithelial Cells.
Aim: To explore the clinical value of miR-193a-5p in neonatal acute respiratory distress syndrome (ARDS) and its role in ARDS cell model in vitro. Methods: RT-qPCR was utilized to detect miR-193a-5p level. Correlation analysis was implemented to assess the correlation between miR-193a-5p and clinical indicators (IL-6, IL-1β, TNF-α, LUS). Human lung epithelial cells induced by LPS were used to construct ARDS cell model. The effects of miR-193a-5p on cell viability, apoptosis and inflammation were evaluated by CCK-8, flow cytometry and ELISA. The target gene of miR-193a-5p was predicted and verified by StarBaseV2.0 and luciferase reporter gene, respectively. Results: MiR-193a-5p level in the ARDS group was down-regulated. MiR-193a-5p levels were negatively correlated with clinical indicators. In vitro studies revealed that up-regulation of miR-193a-5p significantly improved LPS-induced apoptosis, inflammation and viability inhibition. Conclusion: The expression of miR-193a-5p was decreased in neonatal ARDS, it is negatively correlated with the pro-inflammatory factors levels.
期刊介绍:
Fetal and Pediatric Pathology is an established bimonthly international journal that publishes data on diseases of the developing embryo, newborns, children, and adolescents. The journal publishes original and review articles and reportable case reports.
The expanded scope of the journal encompasses molecular basis of genetic disorders; molecular basis of diseases that lead to implantation failures; molecular basis of abnormal placentation; placentology and molecular basis of habitual abortion; intrauterine development and molecular basis of embryonic death; pathogenisis and etiologic factors involved in sudden infant death syndrome; the underlying molecular basis, and pathogenesis of diseases that lead to morbidity and mortality in newborns; prenatal, perinatal, and pediatric diseases and molecular basis of diseases of childhood including solid tumors and tumors of the hematopoietic system; and experimental and molecular pathology.