妊娠大鼠胎盘中未折叠蛋白反应(UPR)的氧化还原谱和介质。

IF 1.8 4区 生物学 Q3 DEVELOPMENTAL BIOLOGY
Jeane Martinha Dos Anjos Cordeiro, Luciano Cardoso Santos, Bianca Reis Santos, Emilly Oliveira Santos, Acácia Eduarda de Jesus Nascimento, Gustavo José Cota de Freitas, Junya de Lacorte Singulani, Daniel de Assis Santos, Mário Sérgio Lima de Lavor, Juneo Freitas Silva
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引用次数: 0

摘要

背景:滋养层细胞的增殖、分化、迁移和凋亡受到缺氧的影响,同时也受到氧化应激和未折叠蛋白反应(UPR)途径的充分调节。目的:我们旨在评估氧化还原和UPR介质在大鼠妊娠期间胎盘中的表达谱。方法:测定Wistar大鼠胎盘缺氧诱导因子1α (HIF1α)、8-羟基-2′-脱氧鸟苷(8-OHdG)、超氧化物歧化酶1 (SOD1)、谷胱甘肽过氧化物酶(GPX)、过氧化氢酶(Cat)、活化转录因子6 (ATF6)、蛋白激酶rna样内质网激酶(PERK)、78 kD葡萄糖调节蛋白(GRP78)和C/ ebp同源蛋白(CHOP)的表达,以及活性氧(ROS)和过氧亚硝酸酯的产生。妊娠第16、18天(DP)。关键结果:在第16和18个DP时,HIF1α免疫染色增加,而在第14个DP时,8-OHdG和ROS的产生增加。SOD1和Cat在第14和18 DP时免疫染色增加,而GPX1/2、GRP78和CHOP在第18 DP时染色增加。基因表达方面,Hif1α和Sod1在第12和16 DP时mRNA表达增加,Gpx1在第10和16 DP时mRNA表达增加。Cat、Perk和Grp78基因在第14个DP的表达量较高,而Atf6在第12个DP的表达量较高。相比之下,Chop在第12至第18 DP期间表达增加。结论:大鼠胎盘氧化还原和UPR介质的表达受胎龄的影响,在HIF1α和8-OHdG表达较高的时期和妊娠末期表达较高。意义:本研究为大鼠胎盘发育过程中氧化还原和UPR介质的生理调节提供了数据。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Redox profile and mediators of the unfolded protein response (UPR) in the placenta of rats during pregnancy.

Context: Proliferation, differentiation, migration and apoptosis of trophoblastic cells are influenced by hypoxia, as well as adequate modulation of oxidative stress and the unfolded protein response (UPR) pathway.

Aims: We aimed to evaluate the expression profile of redox and UPR mediators in the placenta of rats throughout pregnancy.

Methods: Placental expression of hypoxia-inducible factor 1α (HIF1α), 8-Hydroxy-2'-deoxyguanosine (8-OHdG), superoxide dismutase 1 (SOD1), glutathione peroxidase (GPX), catalase (Cat), activating transcription factor 6 (ATF6), protein kinase RNA-like endoplasmic reticulum kinase (PERK), 78 kD glucose-regulated protein (GRP78) and C/EBP-homologous protein (CHOP), as well as reactive oxygen species (ROS) and peroxynitrite production, were evaluated in Wistar rats on the 10th, 12th, 14th, 16th and 18th day of pregnancy (DP).

Key results: Increased immunostaining of HIF1α was observed on the 16th and 18th DP, while 8-OHdG and ROS production were greater on the 14th DP. SOD1 and Cat had increased immunostaining on the 14th and 18th DP, while staining of GPX1/2, GRP78 and CHOP was greater on the 18th DP. With regard to gene expression, Hif1α and Sod1 showed increased mRNA expression on the 12th and 16th DP, while Gpx1 had increased expression on the 10th and 16th DP. Cat , Perk and Grp78 gene expression was greater on the 14th DP, unlike Atf6 , which showed greater expression on the 12th DP. In contrast, Chop maintained increased expression from the 12th to the 18th DP.

Conclusions: The placental expression of redox and UPR mediators in rats is influenced by gestational age, with greater expression in periods of greater HIF1α and 8-OHdG expression and at the end of the pregnancy.

Implications: This study provides data on the physiological modulation of redox and UPR mediators during placental development in rats.

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来源期刊
CiteScore
2.10
自引率
10.50%
发文量
317
审稿时长
2 months
期刊介绍: Reproduction, Fertility and Development is an international journal for the publication of original and significant contributions on vertebrate reproductive and developmental biology. Subject areas include, but are not limited to: physiology, biochemistry, cell and molecular biology, endocrinology, genetics and epigenetics, behaviour, immunology and the development of reproductive technologies in humans, livestock and wildlife, and in pest management. Reproduction, Fertility and Development is a valuable resource for research scientists working in industry or academia on reproductive and developmental biology, clinicians and veterinarians interested in the basic science underlying their disciplines, and students. Reproduction, Fertility and Development is the official journal of the International Embryo Technology Society and the Society for Reproductive Biology. Reproduction, Fertility and Development is published with the endorsement of the Commonwealth Scientific and Industrial Research Organisation (CSIRO) and the Australian Academy of Science.
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