Postpartum increases in cerebral edema and inflammation in response to placental ischemia during pregnancy.
Postpartum increases in cerebral edema and inflammation in response to placental ischemia during pregnancy.
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DOI：
10.1016/j.bbi.2018.03.028
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发表时间：
2018-05
期刊：
影响因子：
--
通讯作者：
Warrington JP
中科院分区：
文献类型：
--
作者：
Clayton AM;Shao Q;Paauw ND;Giambrone AB;Granger JP;Warrington JP
胎盘血流减少导致胎盘缺血，这是先兆子痫（一种高血压妊娠疾病）病理生理学的起始事件。虽然研究表明，有先兆子痫病史的妇女患阿尔茨海默病、中风和脑血管并发症的死亡风险增加，但其潜在机制尚不清楚。在妊娠期间，降低子宫灌注压（RUPP）引起的胎盘缺血导致脑水肿和血脑屏障（BBB）通透性增加;然而，这些并发症是否在分娩后持续存在尚不清楚。因此，我们检验了胎盘缺血导致产后脑水肿和神经炎症的假设。在妊娠第14天，时间妊娠的Sprague道利大鼠进行假手术（n=10）或RUPP（n=9）手术，并在分娩后2个月收集脑组织。RUPP后皮质含水量增加，但海马、纹状体或前脑含水量不增加。使用大鼠细胞因子复合试剂盒，RUPP后后皮质IL-17、IL-1α、IL-1β、Leptin和MIP 2增加，而海马IL-4、IL-12（p70）和RANTES增加，IL-18减少。蛋白质印迹分析显示星形胶质细胞标记物胶质纤维酸性蛋白（GFAP）没有变化，但是，小胶质细胞标记物，离子钙结合接头分子（Iba 1）倾向于增加在海马的RUPP暴露大鼠。免疫荧光染色显示RUPP后皮质小胶质细胞数量减少，但激活（4型）小胶质细胞增加。星形胶质细胞数量增加，在这两个地区，但面积增加，星形胶质细胞仅在后皮质RUPP。血脑屏障相关蛋白，Claudin-1，水通道蛋白-4，和小带occludens-1的表达没有改变，但是，后皮质occludin减少。这些结果表明，产后2个月，神经炎症，沿着occludin表达减少，可能部分解释胎盘缺血史大鼠后皮质水肿。
Reduced placental blood flow results in placental ischemia, an initiating event in the pathophysiology of preeclampsia, a hypertensive pregnancy disorder. While studies show increased mortality risk from Alzheimer’s disease, stroke, and cerebrovascular complications in women with a history of preeclampsia, the underlying mechanisms are unknown. During pregnancy, placental ischemia, induced by reducing uterine perfusion pressure (RUPP), leads to cerebral edema and increased blood-brain barrier (BBB) permeability; however whether these complications persist after delivery is not known. Therefore, we tested the hypothesis that placental ischemia contributes to postpartum cerebral edema and neuroinflammation. On gestational day 14, time-pregnant Sprague Dawley rats underwent Sham (n=10) or RUPP (n=9) surgery and brain tissue collected 2 months post-delivery. Water content increased in posterior cortex but not hippocampus, striatum, or anterior cerebrum following RUPP. Using a rat cytokine multi-plex kit, posterior cortical IL-17, IL-1α, IL-1β, Leptin, and MIP2 increased while hippocampal IL-4, IL-12(p70) and RANTES increased and IL-18 decreased following RUPP. Western blot analysis showed no changes in astrocyte marker, Glial Fibrillary Acidic Protein (GFAP); however, the microglia marker, ionized calcium binding adaptor molecule (Iba1) tended to increase in hippocampus of RUPP-exposed rats. Immunofluorescence staining revealed reduced number of posterior cortical microglia but increased activated (Type 4) microglia in RUPP. Astrocyte number increased in both regions but area covered by astrocytes increased only in posterior cortex following RUPP. BBB-associated proteins, Claudin-1, Aquaporin-4, and zonular occludens-1 expression were unaltered; however, posterior cortical occludin decreased. These results suggest that 2 months postpartum, neuroinflammation, along with decreased occludin expression, may partly explain posterior cortical edema in rats with history of placental ischemia.
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DOI：
10.1161/hypertensionaha.113.01514
发表时间：
2013-12
期刊：
Hypertension (Dallas, Tex. : 1979)
影响因子：
--
作者：
Cornelius DC;Hogg JP;Scott J;Wallace K;Herse F;Moseley J;Wallukat G;Dechend R;LaMarca B
通讯作者：
LaMarca B
DOI：
10.1136/bmj.f894
发表时间：
2013-02-25
期刊：
BMJ (Clinical research ed.)
影响因子：
--
作者：
Bramham, Kate;Nelson-Piercy, Catherine;Chappell, Lucy C
通讯作者：
Chappell, Lucy C
影响因子：
8.3
作者：
Gadonski, Giovani;Babbette, B.;Granger, Joey P.
通讯作者：
Granger, Joey P.
影响因子：
2.3
作者：
Amash, Alaa;Holcberg, Gershon;Huleihel, Mahmoud
通讯作者：
Huleihel, Mahmoud
影响因子：
1.5
作者：
Harmon A;Cornelius D;Amaral L;Paige A;Herse F;Ibrahim T;Wallukat G;Faulkner J;Moseley J;Dechend R;LaMarca B
通讯作者：
LaMarca B