A clinical and in-silico study exploring the association of CASP-3, NF-kB, miR-187, and miR-146 in pre-eclampsia.

IF 2.1 4区 医学 Q3 OBSTETRICS & GYNECOLOGY Hypertension in Pregnancy Pub Date : 2021-11-01 Epub Date: 2021-11-02 DOI:10.1080/10641955.2021.1983592
Charu Sharma, Purvi Purohit, Manoj Khokhar, Anupama Modi, Pratibha Singh, Shashank Shekhar, Shailja Sharma, Meenakshi Gothwal, Praveen Sharma
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引用次数: 1

Abstract

Introduction: Apoptosis is involved in pathogenesis of Pre-eclampsia (PE), further research is needed to determine its molecular mechanism.

Methods: The study recruited two groups (controls; 09, PE; 11). Biochemical tests, RT-PCR and ELISA were employed for analysis of genes and MicroRNAs (miRNA). Bioinformatics tools were employed for interactomics analysis.

Results: There was increased apoptosis in maternal placental tissue (MPT) and Maternal Blood Cells (MBC) as demonstrated by expression of CASP3 and NF-κB1. miR-146-5p and 187-5p were downregulated in MBC and MPT but upregulated in fetal placental tissue (FPT)..

Discussion: An increased apoptosis in MBC and MPT is a significant contributory factor for PE in pregnancy, while FPT is immune to the aforementioned effects.

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一项临床和计算机研究探讨了CASP-3、NF-kB、miR-187和miR-146在先兆子痫中的相关性。
导读:细胞凋亡参与子痫前期(Pre-eclampsia, PE)的发病过程,其分子机制有待进一步研究。方法:研究招募两组(对照组;09年,体育;11)。采用生化试验、RT-PCR和ELISA分析基因和MicroRNAs (miRNA)。生物信息学工具用于相互作用组学分析。结果:小鼠胎盘组织(MPT)和母血细胞(MBC)凋亡明显增加,CASP3和NF-κB1表达明显增加。miR-146-5p和187-5p在MBC和MPT中下调,而在胎儿胎盘组织(FPT)中上调。讨论:MBC和MPT细胞凋亡增加是妊娠PE的重要因素,而FPT不受上述影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Hypertension in Pregnancy
Hypertension in Pregnancy 医学-妇产科学
CiteScore
3.40
自引率
0.00%
发文量
21
审稿时长
6 months
期刊介绍: Hypertension in Pregnancy is a refereed journal in the English language which publishes data pertaining to human and animal hypertension during gestation. Contributions concerning physiology of circulatory control, pathophysiology, methodology, therapy or any other material relevant to the relationship between elevated blood pressure and pregnancy are acceptable. Published material includes original articles, clinical trials, solicited and unsolicited reviews, editorials, letters, and other material deemed pertinent by the editors.
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