妊娠期高血压增加儿童和小鼠癫痫发作的风险。

Baojian Xue,Serena B Gumusoglu,Grant Tiarks,Brittany P Todd,Angela Wong,Donna A Santillan,Chin-Chi Kuo,Hsiu-Yin Chiang,Rohith Ravindranath,Sophia Y Wang,Vinit B Mahajan,Alan Kim Johnson,Heath A Davis,Polly Ferguson,Elizabeth A Newell,Mark K Santillan,Jason M Misurac,Alexander G Bassuk
{"title":"妊娠期高血压增加儿童和小鼠癫痫发作的风险。","authors":"Baojian Xue,Serena B Gumusoglu,Grant Tiarks,Brittany P Todd,Angela Wong,Donna A Santillan,Chin-Chi Kuo,Hsiu-Yin Chiang,Rohith Ravindranath,Sophia Y Wang,Vinit B Mahajan,Alan Kim Johnson,Heath A Davis,Polly Ferguson,Elizabeth A Newell,Mark K Santillan,Jason M Misurac,Alexander G Bassuk","doi":"10.1172/jci183393","DOIUrl":null,"url":null,"abstract":"Gestational hypertension (GH) is prevalent, with life-long health burdens for mothers and their children exposed in utero. We analyzed the nation-wide Epic Cosmos dataset and found significantly higher rates of seizures in children of mothers with GH than in children of normotensive mothers. Complementary studies of nested Iowa and Stanford cohorts and a large Taiwanese cohort also revealed significantly increased seizure risk after covariate adjustments. We modeled this association in an angiotensin (ANG) II mouse model of GH. Maternal ANG II significantly increased seizure grade and deaths elicited by pilocarpine among male but not female offspring. Electrical stimulation increased seizure grade and death across sexes in offspring from ANG II-treated dams. Proinflammatory and microglial gene expression in the brain were upregulated only in male offspring from ANG II-treated dams. Chronic phenylephrine, a GH model lacking the maternal proinflammatory aspects of ANG II, induced similar offspring seizure phenotypes. PLX5622-induced depletion of microglia or antiinflammatory pentoxifylline abolished this sensitized seizure response and lowered mortality in the ANG II model. These results suggest that GH programs offspring risk for seizures in a sex-dependent manner in humans and mice. Neuroinflammatory mechanisms may contribute to the elevated sensitivity and mortality from seizures elicited by GH exposure in utero.","PeriodicalId":520097,"journal":{"name":"The Journal of Clinical Investigation","volume":"13 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Gestational hypertension increases risk of seizures in children and mice.\",\"authors\":\"Baojian Xue,Serena B Gumusoglu,Grant Tiarks,Brittany P Todd,Angela Wong,Donna A Santillan,Chin-Chi Kuo,Hsiu-Yin Chiang,Rohith Ravindranath,Sophia Y Wang,Vinit B Mahajan,Alan Kim Johnson,Heath A Davis,Polly Ferguson,Elizabeth A Newell,Mark K Santillan,Jason M Misurac,Alexander G Bassuk\",\"doi\":\"10.1172/jci183393\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Gestational hypertension (GH) is prevalent, with life-long health burdens for mothers and their children exposed in utero. We analyzed the nation-wide Epic Cosmos dataset and found significantly higher rates of seizures in children of mothers with GH than in children of normotensive mothers. Complementary studies of nested Iowa and Stanford cohorts and a large Taiwanese cohort also revealed significantly increased seizure risk after covariate adjustments. We modeled this association in an angiotensin (ANG) II mouse model of GH. Maternal ANG II significantly increased seizure grade and deaths elicited by pilocarpine among male but not female offspring. Electrical stimulation increased seizure grade and death across sexes in offspring from ANG II-treated dams. Proinflammatory and microglial gene expression in the brain were upregulated only in male offspring from ANG II-treated dams. Chronic phenylephrine, a GH model lacking the maternal proinflammatory aspects of ANG II, induced similar offspring seizure phenotypes. PLX5622-induced depletion of microglia or antiinflammatory pentoxifylline abolished this sensitized seizure response and lowered mortality in the ANG II model. These results suggest that GH programs offspring risk for seizures in a sex-dependent manner in humans and mice. Neuroinflammatory mechanisms may contribute to the elevated sensitivity and mortality from seizures elicited by GH exposure in utero.\",\"PeriodicalId\":520097,\"journal\":{\"name\":\"The Journal of Clinical Investigation\",\"volume\":\"13 1\",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2025-06-16\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"The Journal of Clinical Investigation\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1172/jci183393\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"The Journal of Clinical Investigation","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1172/jci183393","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

摘要

妊娠期高血压(GH)是普遍存在的,与终身健康负担的母亲和他们的孩子暴露在子宫内。我们分析了全国范围内的史诗宇宙数据集,发现生长激素母亲的孩子癫痫发作率明显高于正常母亲的孩子。对爱荷华州和斯坦福大学嵌套队列以及台湾大型队列的补充研究也显示,协变量调整后癫痫发作风险显著增加。我们在血管紧张素(ANG) II小鼠GH模型中模拟了这种关联。在雄性后代中,母体angii显著增加了匹罗卡平引起的癫痫发作等级和死亡,而雌性后代则没有。电刺激增加了angii处理过的水坝后代的癫痫发作等级和死亡率。仅在angii处理的雄性后代中,大脑中的促炎和小胶质基因表达上调。慢性苯肾上腺素,一种缺乏母体angii促炎方面的生长激素模型,诱导了类似的后代癫痫表型。在ANG II模型中,plx5622诱导的小胶质细胞或抗炎戊氧可可碱的消耗消除了这种致敏的癫痫发作反应,降低了死亡率。这些结果表明,生长激素在人类和小鼠中以性别依赖的方式控制后代癫痫发作的风险。神经炎症机制可能有助于提高敏感性和死亡率癫痫发作由生长激素暴露在子宫。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Gestational hypertension increases risk of seizures in children and mice.
Gestational hypertension (GH) is prevalent, with life-long health burdens for mothers and their children exposed in utero. We analyzed the nation-wide Epic Cosmos dataset and found significantly higher rates of seizures in children of mothers with GH than in children of normotensive mothers. Complementary studies of nested Iowa and Stanford cohorts and a large Taiwanese cohort also revealed significantly increased seizure risk after covariate adjustments. We modeled this association in an angiotensin (ANG) II mouse model of GH. Maternal ANG II significantly increased seizure grade and deaths elicited by pilocarpine among male but not female offspring. Electrical stimulation increased seizure grade and death across sexes in offspring from ANG II-treated dams. Proinflammatory and microglial gene expression in the brain were upregulated only in male offspring from ANG II-treated dams. Chronic phenylephrine, a GH model lacking the maternal proinflammatory aspects of ANG II, induced similar offspring seizure phenotypes. PLX5622-induced depletion of microglia or antiinflammatory pentoxifylline abolished this sensitized seizure response and lowered mortality in the ANG II model. These results suggest that GH programs offspring risk for seizures in a sex-dependent manner in humans and mice. Neuroinflammatory mechanisms may contribute to the elevated sensitivity and mortality from seizures elicited by GH exposure in utero.
求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信