Transcriptomic survey of key reproductive and metabolic tissues in mouse models of polycystic ovary syndrome.
Yu PeiSanjiv RisalHong JiangHaojiang LuEva LindgrenElisabet Stener-VictorinQiaolin DengPublished in: Communications biology (2023)
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.
Keyphrases
- polycystic ovary syndrome
- insulin resistance
- adipose tissue
- high fat diet induced
- high fat diet
- mouse model
- metabolic syndrome
- growth factor
- single cell
- skeletal muscle
- genome wide
- gene expression
- type diabetes
- signaling pathway
- rna seq
- multiple sclerosis
- pregnancy outcomes
- transcription factor
- induced apoptosis
- pi k akt
- nuclear factor
- lps induced
- genome wide identification
- oxidative stress
- weight loss
- mass spectrometry
- pregnant women
- cell cycle arrest
- cell proliferation
- dna methylation
- ms ms
- computed tomography
- inflammatory response
- magnetic resonance imaging
- genome wide analysis