eNOS/iNOS and endoplasmic reticulum stress-induced apoptosis in the placentas of patients with preeclampsia.
eNOS/iNOS and endoplasmic reticulum stress-induced apoptosis in the placentas of patients with preeclampsia.
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先兆子痫患者胎盘中 eNOS/iNOS 和内质网应激诱导的细胞凋亡
DOI：
10.1038/jhh.2016.17
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发表时间：
2017-01
影响因子：
2.7
通讯作者：
中科院分区：
文献类型：
--
作者：
在子痫前期（PE）中观察到一氧化氮通路的破坏和内质网（ER）应激。然而，ER应激相关标志物和内皮型一氧化氮合酶/诱导型一氧化氮合酶（eNOS/iNOS）在PE患者中的相关性和总体详细表达谱知之甚少。在这项研究中，ER应激相关标志物的胎盘蛋白表达以及eNOS/iNOS在正常血压对照组（n= 32）和PE妊娠（n= 32）进行了检测。此外，凋亡检测的末端脱氧核苷酸转移酶介导的缺口末端标记（TUNEL）染色胎盘。与对照组相比，我们发现PE患者胎盘组织中ER应激反应的升高与iNOS的上调相一致。ER应激相关标志物的胎盘蛋白表达，包括GRP 78、GRP 94、p-PERK、eIF 2a、p-eIF 2a、XBP 1、CHOP、Ire 1、p-Ire 1和iNOS，在PE组中较高，eNOS表达较低（P均< 0.05）;然而，在PE组和对照组中，ATF 6和PERK的表达相似。PE胎盘组织中CHOP和iNOS的表达上调与TUNEL染色显示的细胞凋亡增加和caspase 4表达上调一致。我们的数据表明，过度的ER应激反应和上调的iNOS可能与PE患者胎盘细胞凋亡增加有关，并可能有助于PE的病理生理学。
Disruption of nitric oxide pathway and endoplasmic reticulum (ER) stress had been observed in preeclampsia (PE). However, the correlation and overall detailed expression profiles of ER stress-related markers and endothelial nitric oxide synthase/inducible nitric oxide synthase (eNOS/iNOS) in patients with PE were poorly understood. In this study, placental protein expression of ER stress-related markers as well as eNOS/iNOS in normotensive control (n= 32) and PE pregnancies (n= 32) was examined by western blot. In addition, apoptosis was detected by terminal deoxynucleotidyl transferase-mediated nick-end labelling (TUNEL) staining in placentas. Compared with control, we found elevated ER stress response was agreeable with iNOS upregulation in placenta tissue of PE patients. Placental protein expression of ER stress-related markers, including GRP78, GRP94, p-PERK, eIF2a, p-eIF2a, XBP1, CHOP, Ire1, p-Ire1 and iNOS, was higher, and eNOS expression was lower in PE (P< 0.05 for all); however, the expression of ATF6 and PERK was similar in the PE and control groups. Upregulation of CHOP and iNOS was consistent of apoptosis increasing indicated by TUNEL staining and caspase 4 expression upregulation in PE placenta. Our datas suggest that the exaggerated ER stress response and upregulated iNOS are probably associated with increased apoptosis in placenta of PE patients and may contribute to the pathophysiology of PE.
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