The following is a summary of “Role of lncRNA-MEG8/miR-296-3p axis in gestational diabetes mellitus” published in the September 2022 issue of Nephrology by Bian et al.
Most pregnancies end in gestational diabetes mellitus (GDM), which is a frequent consequence. Long-noncoding RNA maternally expressed 8 (lncRNA-MEG8) mechanisms and effects on gestational diabetes mellitus were the subjects of the study.
StarBase software was used to make early predictions about specific interactions between lncRNA-MEG8 and miR-296-3p, and dual-luciferase reporter gene analysis was used to confirm those predictions. Using reverse transcription-quantitative polymerase chain reaction, the expression levels of lncRNA-MEG8 and miR-296-3p in peripheral blood samples from individuals with GDM were determined. To assess the total levels of insulin and insulin secretion, an enzyme-linked immunosorbent assay was performed. Cell viability and apoptosis were also determined using MTT and flow cytometric techniques. Western blotting was used to identify the proteins linked to cell apoptosis.
The findings suggested that miR-296-3p may target lncRNA-MEG8. Compared to healthy people, patients with GDM had greater levels of lncRNA-MEG8 and lower levels of miR-296-3p. Insulin secretion and content were increased by LncRNA-MEG8-siRNA. Additionally, MEG8-siRNA reduced apoptosis and raised cell viability. A miR-296-3p inhibitor, however, prevented these modifications from occurring. Additionally, INS-1 cells responded to a miR-296-3p mimic like that of MEG8-siRNA, as shown by improved insulin production, increased cell survival, and decreased apoptosis.
LncRNA-MEG8-siRNA enhanced miR-296-3p, which was necessary for pancreatic beta-cell activity.