Effect of microRNA-186 on oxidative stress injury of neuron by targeting interleukin 2 through the janus kinase-signal transducer and activator of transcription pathway in a rat model of Alzheimer's disease
JOURNAL OF CELLULAR PHYSIOLOGY
Authors: Wu, Dong-Mei; Wen, Xin; Wang, Yong-Jian; Han, Xin-Rui; Wang, Shan; Shen, Min; Fan, Shao-Hua; Zhuang, Juan; Zhang, Zi-Feng; Shan, Qun; Li, Meng-Qiu; Hu, Bin; Sun, Chun-Hui; Lu, Jun; Chen, Gui-Quan; Zheng, Yuan-Lin
Abstract
Recent studies have proposed that microRNAs (miR) function as novel diagnostic and prognostic biomarkers and therapeutic targets in Alzheimer's disease (AD), a common disease among the elderly. In the current study, we aim to explore the effect of miR-186 on oxidative stress injury of neuron in rat models ofAD with the involvement of the interleukin-2 (IL2) and the Janus kinase/signal transducers and activators of transcription (JAK-STAT) pathways. AD rat models were established, and dual-luciferase reporter assay and online software were used to confirm the targeting relationship between miR-186 and IL2. Immunohistochemistry was usedevaluating the positive rate of IL2. Afterward, to define the role of miR-186 in AD, miR-186, IL2, and JAK-STAT related protein (JAK2, STAT3) expressions were quantified. Cell proliferation was measured by 3-(4,5-dimethylthiazol-2-yl)2,5-diphenyl tetrazolium bromide, and cell apoptosis was detected by flow cytometry. We observed downregulated miR-186 and IL2 and upregulated JAK-STAT signaling pathway related genes in AD. The overexpression of miR-186 was shown to significantly promote cell proliferation while suppressing cell apoptosis along with the expression of the IL2 and JAK-STAT signaling pathway related protein. Collectively, the key findings obtained from the current study define the potential role of miR-186 as an inhibitor of AD development by downregulation of IL2 through suppression of the JAK-STAT signaling pathway.
Amniotic immune biomarkers as risk factors in women with different symptoms of threatened late miscarriage
AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY
Authors: Meng, Lili; Wang, Zhenhua; Reilly, Marie; Zhang, Shuning; Liu, Xiuli; Lin, Dijin; Liu, Shengxin; Liu, Yinglin; Zhang, Jianping; Chen, Hui
Abstract
Problem To investigate risk factors that can help identify the possibility of pregnancy loss in threatened late miscarriage (TLM) patients with and without spontaneous uterine contractions. Method of study Amniotic immune biomarkers (IL2 beta receptor, IL6, IL8, IL10, IL1 beta, and TNF alpha) were assayed, and "sludge" was assessed. Patients without intrauterine infections were treated and followed up until delivery, and pregnancy outcomes were recorded. The two groups were compared for the differences in biomarker levels and "sludge," and the independent associations of biomarkers, "sludge," and other maternal factors with late miscarriage were investigated. Results The amniotic levels of IL2 beta R, IL8, and TNF alpha were higher in the group with contractions (P < .05). When considered alone, each of the six biomarkers was significantly associated with late miscarriage in the no-contractions group and four of these (IL8, IL10, IL1 beta, and TNF alpha) in the contractions group (P < .05). Biomarker levels were correlated, and in multivariate Cox regression analysis, there was an independent effect only for IL8 in the no-contractions group (HR = 18.16, 95% CI: 5.75-57.43) and TNF alpha in the contractions group (HR = 4.11, 95% CI: 1.68-10.08). For patients with contractions, IL10, IL8, and IL1 beta were different in those with and without "sludge," but no such difference was seen in the no-contractions group. Conclusion For TLM patients without intrauterine infections, amniotic immune biomarkers differ between patients with different symptoms, not only for their levels but also for the impact of these biomarkers on the risk of late miscarriage. These findings suggest that the symptoms of TLM should be considered in the study of miscarriage risk.