Aims: Gestational diabetes mellitus (GDM)-induced macrosomia is predominantly characterized by fat accumulation, which is closely related to adipocyte differentiation. An unknown long noncoding RNA RP11-290L1.3, referred to as RP11, was identified to be dramatically upregulated in the umbilical cord blood of women with GDM-induced macrosomia in our previous study. We conducted this study to identify the function of RP11 in GDM-induced macrosomia.
Methods: The effects of RP11 gain- and loss-of-function on HPA-v (human preadipocytes-visceral) adipogenesis were determined with lentivirus mediated cell transduction. The mRNA and protein expression levels of adipogenesis makers were evaluated by qPCR/western blot. Then, we performed the Microarray and pathway analysis to explore the possible mechanisms by which RP11 regulates adipogenesis.
Results: Overexpression of RP11 significantly enhanced adipocyte differentiation and increased the mRNA and protein expression levels of adipogenesis makers, such as PPAR-γ, SREBP1c, and FASN by qPCR/western blot. Knockdown of RP11 showed opposite effects. Microarray and pathway analysis showed, after RP11 knockdown, 1,612 genes were upregulated and 583 genes were downregulated which were found to be mainly involved in metabolic pathways, insulin signaling pathway and MAPK signaling pathway.
Conclusion: In conclusion, the unknown lncRNA RP11 serves a positive factor on preadipocyte differentiation which could shed light on fetal fat accumulation in GDM.