Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
Center for molecular medicine, Karolinska University Hospital, Stockholm, Sweden.
Commun Biol. 2023 Jan 18;6(1):69. doi: 10.1038/s42003-022-04362-0.
Excessive androgen production and obesity are key to polycystic ovary syndrome (PCOS) pathogenesis. Prenatal androgenized (PNA), peripubertal androgenized, and overexpression of nerve growth factor in theca cells (17NF) are commonly used PCOS-like mouse models and diet-induced maternal obesity model is often included for comparsion. To reveal the molecular features of these models, we have performed transcriptome survey of the hypothalamus, adipose tissue, ovary and metaphase II (MII) oocytes. The largest number of differentially expressed genes (DEGs) is found in the ovaries of 17NF and in the adipose tissues of peripubertal androgenized models. In contrast, hypothalamus is most affected in PNA and maternal obesity models suggesting fetal programming effects. The Ms4a6e gene, membrane-spanning 4-domains subfamily A member 6E, a DEG identified in the adipose tissue in all mouse models is also differently expressed in adipose tissue of women with PCOS, highlighting a conserved disease function. Our comprehensive transcriptomic profiling of key target tissues involved in PCOS pathology highlights the effects of developmental windows for androgen exposure and maternal obesity, and provides unique resource to investigate molecular mechanisms underlying PCOS pathogenesis.
雄激素产生过多和肥胖是多囊卵巢综合征(PCOS)发病机制的关键。产前雄激素化(PNA)、青春期前雄激素化和颗粒细胞中神经生长因子过表达(17NF)是常用的多囊卵巢综合征样小鼠模型,并且通常包括饮食诱导的母体肥胖模型进行比较。为了揭示这些模型的分子特征,我们对下丘脑、脂肪组织、卵巢和中期 II(MII)卵母细胞进行了转录组调查。在 17NF 的卵巢和青春期前雄激素化模型的脂肪组织中发现了最多数量的差异表达基因(DEGs)。相比之下,在 PNA 和母体肥胖模型中,下丘脑受到的影响最大,表明存在胎儿编程效应。Ms4a6e 基因,跨膜 4 结构域亚家族 A 成员 6E,是在所有小鼠模型的脂肪组织中鉴定出的 DEG,在 PCOS 妇女的脂肪组织中也有不同的表达,突出了保守的疾病功能。我们对涉及 PCOS 病理的关键靶组织的全面转录组分析突出了雄激素暴露和母体肥胖的发育窗口期的影响,并为研究 PCOS 发病机制的分子机制提供了独特的资源。