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子痫前期胎盘和脐带中的凋亡和应激信号标记物增加。

Apoptotic and stress signaling markers are augmented in preeclamptic placenta and umbilical cord.

作者信息

Afroze Syeda H, Kalagiri Ram R, Reyes Michelle, Zimmerman Jacqueline D, Beeram Madhava R, Drever Nathan, Zawieja David C, Kuehl Thomas J, Uddin Mohammad N

机构信息

Department of Medical Physiology, Texas A&M Health Science Center College of Medicine, Temple, TX, USA.

Department of Pediatrics, Baylor Scott & White Health, Texas A&M Health Science Center College of Medicine, Temple, TX, USA.

出版信息

BBA Clin. 2016 May 25;6:25-30. doi: 10.1016/j.bbacli.2016.05.003. eCollection 2016 Dec.

DOI:10.1016/j.bbacli.2016.05.003
PMID:27335802
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4906135/
Abstract

OBJECTIVE

Preeclampsia (preE) has a significant link to alterations of placental function leading to stress and apoptotic signaling, which pass the placental barrier and leave persistent defect in the circulation of the offspring. We assessed apoptotic signaling in placentas and umbilical cords from patients with and without preE.

METHODS

We collected placental and cord tissues from 27 normal pregnant (NP) women and 20 preE consenting patients after delivery in an IRB approved prospective study. p38 mitogen-activated protein kinase (p38 MAPK) phosphorylation, pro-apoptotic Bcl-2-associated X (Bax), anti-apoptotic Bcl-2, caspase-9, and pro-inflammatory cyclooxygenase-2 (Cox-2) were evaluated by western blot and immunohistochemistry. Comparisons were performed using Student's t-test.

RESULTS

p38 phosphorylation (Placenta: 1.5 fold, Cord: 1.7 fold), ratio of Bax/Bcl-2 (Placenta: 1.7 fold, Cord: 2.2 fold), caspase-9 (Placenta: 1.5 fold, Cord: 1.8 fold) and Cox-2 (Placenta: 2.5 fold, Cord: 2.3 fold) were up-regulated (p < 0.05) in preE compared to NP patients. Average hospital stays for preE babies were longer than NP babies. No complications were reported for NP babies; however, all of preE babies had multiple complications.

CONCLUSIONS

Apoptotic and stress signaling are augmented in preE placenta and cord tissue that alter the intrauterine environment and activates the detrimental signaling that is transported to fetus.

摘要

目的

子痫前期（preE）与胎盘功能改变密切相关，可导致应激和凋亡信号，这些信号穿过胎盘屏障，在子代循环中留下持续性缺陷。我们评估了子痫前期患者和非子痫前期患者胎盘及脐带中的凋亡信号。

方法

在一项经机构审查委员会批准的前瞻性研究中，我们收集了27名正常孕妇（NP）和20名子痫前期患者分娩后的胎盘和脐带组织。通过蛋白质免疫印迹法和免疫组织化学法评估p38丝裂原活化蛋白激酶（p38 MAPK）磷酸化、促凋亡蛋白Bcl-2相关X蛋白（Bax）、抗凋亡蛋白Bcl-2、半胱天冬酶-9和促炎环氧化酶-2（Cox-2）。采用学生t检验进行比较。

结果

与NP患者相比，子痫前期患者的p38磷酸化（胎盘：1.5倍，脐带：1.7倍）、Bax/Bcl-2比值（胎盘：1.7倍，脐带：2.2倍）、半胱天冬酶-9（胎盘：1.5倍，脐带：1.8倍）和Cox-2（胎盘：2.5倍，脐带：2.3倍）上调（p < 0.05）。子痫前期婴儿的平均住院时间比NP婴儿长。NP婴儿未报告并发症；然而，所有子痫前期婴儿都有多种并发症。

结论

子痫前期胎盘和脐带组织中的凋亡和应激信号增强，改变了子宫内环境，并激活了传递给胎儿的有害信号。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d611/4906135/a75a5101cfbc/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d611/4906135/6f0827e62305/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d611/4906135/0f57778a950f/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d611/4906135/b98abfd12c80/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d611/4906135/97aad2dc308a/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d611/4906135/a75a5101cfbc/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d611/4906135/6f0827e62305/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d611/4906135/0f57778a950f/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d611/4906135/b98abfd12c80/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d611/4906135/97aad2dc308a/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d611/4906135/a75a5101cfbc/gr5.jpg

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