Bakhshalizadeh Shabnam, Rabiee Farzaneh, Shirazi Reza, Ghaedi Kamran, Amidi Fardin, Nasr-Esfahani Mohammad Hossein
Department of Anatomy, School of Medicine, Zanjan University of Medical Sciences, Zanjan, Iran.
Department of Cellular Biotechnology, Cell Science Research Center, Royan Institute for Biotechnology, ACECR, Isfahan, Iran.
J Reprod Infertil. 2018 Apr-Jun;19(2):89-94.
Polycystic ovarian syndrome (PCOS) is a metabolic and endocrine disorder which is characterized by hyperandrogenism, anovulation or oligomenorrhea and polycystic ovarian morphology. It is believed that modulation in metabolism of granulosa cells of PCOS patients may lead to infertility. One of the metabolic modulators is FNDC5 and its cleaved form, irisin. The axis of PGC1α-FNDC5 pathway is one of the main factors affecting cellular energy balance the purpose of this study was to evaluate this pathway in granulosa cells derived from PCOS mice model in comparison with control group.
In the present study, PCOS mouse model was developed by injection of dehydroepiandrosterone (DHEA) hormone in 20 mice for a period of 20 days. Also, 20 uninjected mice were used as the control. Meanwhile, a vehicle group consisted of mice which received daily subcutaneous sesame oil injection (n=20). Relative expressions of PGC1α and FNDC5 in granulosa cells were evaluated by RT-qPCR. Analysis of gene expressions was calculated by the ΔΔCT method and the relative levels of mRNA were normalized to GAPDH transcript levels. Differences in genes expression among three groups were assessed using one-way ANOVA, Tukey's Post Hoc test.
Our results showed that expression of FNDC5 was significantly reduced in granulosa cells of DHEA-induced PCOS mice compared with control and vehicle groups (p<0.05), while there was no significant differences in PGC1α expression among different groups.
Down regulation of FNDC5 transcript level may contribute in metabolic disturbance of granulosa cells derived from PCOS ovary apart from PGC1α levels which remained unchanged.
多囊卵巢综合征(PCOS)是一种代谢和内分泌紊乱疾病,其特征为高雄激素血症、无排卵或月经过少以及多囊卵巢形态。据信,PCOS患者颗粒细胞代谢的调节异常可能导致不孕。代谢调节因子之一是FNDC5及其裂解形式鸢尾素。PGC1α-FNDC5通路轴是影响细胞能量平衡的主要因素之一,本研究的目的是评估该通路在PCOS小鼠模型来源的颗粒细胞中与对照组相比的情况。
在本研究中,通过给20只小鼠注射脱氢表雄酮(DHEA)激素20天建立PCOS小鼠模型。另外,20只未注射的小鼠作为对照。同时,设立一个载体组,该组小鼠每天接受皮下注射芝麻油(n = 20)。通过RT-qPCR评估颗粒细胞中PGC1α和FNDC5的相对表达。基因表达分析采用ΔΔCT法计算,mRNA相对水平以GAPDH转录水平进行标准化。使用单因素方差分析、Tukey事后检验评估三组之间基因表达的差异。
我们的结果显示,与对照组和载体组相比,DHEA诱导的PCOS小鼠颗粒细胞中FNDC5的表达显著降低(p<0.05),而不同组之间PGC1α的表达没有显著差异。
除了PGC1α水平保持不变外,FNDC5转录水平的下调可能导致PCOS卵巢来源的颗粒细胞代谢紊乱。