Association of placental PPARα/γ and miR-27b expression with macrosomia in healthy pregnancy

小RNA 巨大儿 胎盘 内科学 内分泌学 信使核糖核酸 过氧化物酶体增殖物激活受体 免疫印迹 生物 男科 受体 下调和上调 怀孕 医学 胎儿 基因 妊娠期 遗传学 妊娠期糖尿病
作者
Li-Fang Ni,Ying Han,Shanshan Wang,Xiao-Jun Lin,Yuhuan Wang,Hongtao Yan,Xinjun Yang
出处
期刊:Pediatric Research [Springer Nature]
卷期号:93 (1): 267-273
标识
DOI:10.1038/s41390-022-02072-1
摘要

BackgroundPeroxisomal proliferator-activated receptors (PPARs) and microRNAs (miRNAs) play important roles in the development of fetuses, whereas expression changes of PPARs and three miRNAs (miR-17, miR-27b and miR-34a) and whether these miRNAs regulate PPARs in non-GDM macrosomia placenta is unclear.MethodsA case–control study was performed to collect information and placental tissues on mothers and newborns of non-GDM macrosomia and normal-birth-weight infants. In vitro HTR8-SVneo cellular model was used to detect the effects of miRNAs on PPARs expression. Quantitative real-time PCR (qRT-PCR) and western blot was applied to examine the expression levels of PPARs, miR-17, miR-27b, and miR-34a in placental tissues and cells.ResultsThe PPARα/γ mRNA and protein levels were significantly up-regulated and miR-27b was down-regulated in the placenta of macrosomia group compared with in the control group, while no difference was observed in PPARβ, miR-17, and miR-34a. After adjusting for confounding factors, low miR-27b and high PPARα/γ mRNA expression still increased the risk of macrosomia. The PPARα/γ protein levels presented a corresponding decrease or increase when cells were transfected with miR-27b mimic or inhibitor.ConclusionsPlacental PPARα/γ and miR-27b expression were associated with non-GDM macrosomia and miR-27b probably promotes the occurrence of non-GDM macrosomia by regulating PPARα/γ protein.Impact Low miR-27b and high PPARα/γ mRNA expression in the placenta were associated with higher risk of macrosomia. In vitro HTR8-SVneo cell experiment supported that miR-27b could negatively regulate the expression of PPARα and PPARγ protein. MiR-27b was probably involved in non-GDM macrosomia through negative regulation of PPARα/γ protein.
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