{"title":"Study on the regulation of trophoblast activity by abnormally expressed hsa_circ_0002768 in patients with gestational diabetes mellitus.","authors":"Qian Liu, Lianzhi Wu","doi":"10.5603/gpl.99058","DOIUrl":null,"url":null,"abstract":"<p><p>O: BJECTIVES: Circular RNAs (circRNAs) are known to be associated with the progression of gestational diabetes mellitus (GDM). Thus, the objective of this study was to unveil the influnce and potential mechanism of hsa_circ_0002768 in GDM. M: ATERIAL AND: METHODS: Levels of hsa_circ_0002768 were quantified by RT-qPCR. Placental hsa_circ_0002768 levels were analyzed after pregnancies. Trophoblast cell (HTR-8/SVneo) functions, including oxidative stress, mitochondrial dysfunction, cell viability, autophagy, and invasion, were evaluated upon hsa_circ_0002768 knockdown. Finally, the downstream miRNA for hsa_circ_0002768 was investigated. RESULTS: Hsa_circ_0002768 levels increased as high glucose-induced, and in GDM placenta. In vitro experiments showed that hsa_circ_0002768 knockdown positively regulated trophoblast oxidative stress and mitochondrial functions, thus inducing cell viability and invasion, but inhibiting autophagy. miR-339-5p was a downstream molecular for hsa_circ_0002768, which targeted to TLE3. CONCLUSIONS: This study reveals a physiological role for hsa_circ_0002768 during GDM.</p>","PeriodicalId":94021,"journal":{"name":"Ginekologia polska","volume":" ","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2025-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Ginekologia polska","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.5603/gpl.99058","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
O: BJECTIVES: Circular RNAs (circRNAs) are known to be associated with the progression of gestational diabetes mellitus (GDM). Thus, the objective of this study was to unveil the influnce and potential mechanism of hsa_circ_0002768 in GDM. M: ATERIAL AND: METHODS: Levels of hsa_circ_0002768 were quantified by RT-qPCR. Placental hsa_circ_0002768 levels were analyzed after pregnancies. Trophoblast cell (HTR-8/SVneo) functions, including oxidative stress, mitochondrial dysfunction, cell viability, autophagy, and invasion, were evaluated upon hsa_circ_0002768 knockdown. Finally, the downstream miRNA for hsa_circ_0002768 was investigated. RESULTS: Hsa_circ_0002768 levels increased as high glucose-induced, and in GDM placenta. In vitro experiments showed that hsa_circ_0002768 knockdown positively regulated trophoblast oxidative stress and mitochondrial functions, thus inducing cell viability and invasion, but inhibiting autophagy. miR-339-5p was a downstream molecular for hsa_circ_0002768, which targeted to TLE3. CONCLUSIONS: This study reveals a physiological role for hsa_circ_0002768 during GDM.