Molecular Microbiology Laboratory, ICMR-National Institute of Pathology, Sriramachari Bhawan, Safdarjung Hospital Campus, Post Box no. 4909, New Delhi, 110029, India.
ICMR Computational Genomics Centre, All India Institute of Medical Sciences, Indian Council of Medical Research, New Delhi, 110029, India.
Sci Rep. 2022 Aug 29;12(1):14688. doi: 10.1038/s41598-022-18941-y.
Study aimed to characterize the expression of antioxidant genes SOD1 and SOD2 in Chlamydia trachomatis-induced recurrent spontaneous aborters and further determine their role by in silico analysis. First void urine was collected from 130 non-pregnant women with history of recurrent spontaneous abortion (RSA) (Group I) and 130 non-pregnant women (Group II; control) attending Obstetrics and Gynecology Department, SJH, New Delhi, India. C. trachomatis detection was performed by conventional PCR in urine. Gene expression of SOD1 and SOD2 was performed by quantitative real-time PCR. Further, its interacting partners were studied by in silico analysis. 22 patients were positive for C. trachomatis in Group I. Significant upregulation was observed for SOD2 gene in C. trachomatis-infected RSA patients while SOD1 was found to be downregulated. Increased concentration of oxidative stress biomarkers 8-hydroxyguanosine and 8-isoprostane was found in C. trachomatis-infected RSA patients. Protein-protein interaction (PPI) of SOD proteins and its interacting partners viz.; CCS, GPX1, GPX2, GPX3, GPX4, GPX5, GPX7, GPX8, CAT, PRDX1, TXN, SIRT3, FOXO3, and AKT1 were found to be involved in MAPK, p53 and foxo signaling pathways. Molecular pathways involved in association with SODs indicate reactive oxygen species (ROS) detoxification, apoptotic pathways and cell cycle regulation. Overall data revealed alleviated levels of SOD2 gene and decreased expression of SOD1 gene in response to C. trachomatis-infection leading to production of oxidative stress and RSA.
本研究旨在分析沙眼衣原体诱导的复发性自然流产患者抗氧化基因 SOD1 和 SOD2 的表达特征，并通过计算机分析进一步确定其作用。首先，从印度新德里 SJH 妇产科就诊的 130 名有复发性自然流产史的非孕妇（I 组）和 130 名非孕妇（II 组；对照组）中收集首次晨尿。采用常规 PCR 法检测尿中沙眼衣原体。采用实时定量 PCR 法检测 SOD1 和 SOD2 的基因表达。进一步通过计算机分析研究其相互作用伙伴。I 组中 22 例患者沙眼衣原体阳性。沙眼衣原体感染的 RSA 患者 SOD2 基因表达显著上调，而 SOD1 基因表达下调。在沙眼衣原体感染的 RSA 患者中发现氧化应激生物标志物 8-羟基鸟嘌呤和 8-异前列腺素的浓度增加。SOD 蛋白及其相互作用伙伴 CCS、GPX1、GPX2、GPX3、GPX4、GPX5、GPX7、GPX8、CAT、PRDX1、TXN、SIRT3、FOXO3 和 AKT1 的蛋白-蛋白相互作用（PPI）被发现参与 MAPK、p53 和 foxo 信号通路。与 SODs 相关的分子途径表明，活性氧（ROS）解毒、凋亡途径和细胞周期调节。总的来说，数据显示沙眼衣原体感染后 SOD2 基因水平降低，SOD1 基因表达下调，导致氧化应激和 RSA 的产生。
