Choroid plexus remodeling associated with inflammatory CSF exposure in preterm acquired hydrocephalus.

IF 4.5 2区综合性期刊 Q1 MULTIDISCIPLINARY SCIENCES

iScience Pub Date : 2026-10-01 eCollection Date: 2026-10-16 DOI:10.1016/j.isci.2026.117759

Gio Jison, Noah Ramos, Fernando Cotrim-Gomes, Seunghyun Lee, Brian W Hanak, Michael Muhonen, Leandro Castañeyra-Ruiz

{"title":"Choroid plexus remodeling associated with inflammatory CSF exposure in preterm acquired hydrocephalus.","authors":"Gio Jison, Noah Ramos, Fernando Cotrim-Gomes, Seunghyun Lee, Brian W Hanak, Michael Muhonen, Leandro Castañeyra-Ruiz","doi":"10.1016/j.isci.2026.117759","DOIUrl":null,"url":null,"abstract":"<p><p>Acquired hydrocephalus in preterm infants follows intraventricular hemorrhage (IVH) or central nervous system infection and is associated with inflammatory cerebrospinal fluid (CSF) profiles. We integrated clinical magnetic resonance imaging (MRI), CSF cytokine profiling, primary human choroid plexus (ChP) epithelial and endothelial cell assays, and independent transcriptomic and proteomic datasets to investigate ChP remodeling. Infants requiring CSF diversion exhibited greater ChP thickness independent of gestational age, ventricular size, and IVH severity, supporting its potential as a biomarker. Growth factor-enriched inflammatory CSF increased proliferation in primary human ChP epithelial and endothelial cells; EGFR and VEGFR inhibition attenuated these responses, and recombinant epidermal growth factor (EGF) and vascular endothelial growth factor (VEGF) reproduced proliferative effects. Independent IVH transcriptomic data confirmed Mki67 elevation in IVH ChP tissue. Integrated proteomic trajectories support a temporally dynamic remodeling framework linking acute inflammatory signaling to proliferative ChP activation and structural remodeling.</p>","PeriodicalId":342,"journal":{"name":"iScience","volume":"29 10","pages":"117759"},"PeriodicalIF":4.5000,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13657226/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"iScience","FirstCategoryId":"103","ListUrlMain":"https://doi.org/10.1016/j.isci.2026.117759","RegionNum":2,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2026/10/16 0:00:00","PubModel":"eCollection","JCR":"Q1","JCRName":"MULTIDISCIPLINARY SCIENCES","Score":null,"Total":0}

引用次数: 0

Abstract

Acquired hydrocephalus in preterm infants follows intraventricular hemorrhage (IVH) or central nervous system infection and is associated with inflammatory cerebrospinal fluid (CSF) profiles. We integrated clinical magnetic resonance imaging (MRI), CSF cytokine profiling, primary human choroid plexus (ChP) epithelial and endothelial cell assays, and independent transcriptomic and proteomic datasets to investigate ChP remodeling. Infants requiring CSF diversion exhibited greater ChP thickness independent of gestational age, ventricular size, and IVH severity, supporting its potential as a biomarker. Growth factor-enriched inflammatory CSF increased proliferation in primary human ChP epithelial and endothelial cells; EGFR and VEGFR inhibition attenuated these responses, and recombinant epidermal growth factor (EGF) and vascular endothelial growth factor (VEGF) reproduced proliferative effects. Independent IVH transcriptomic data confirmed Mki67 elevation in IVH ChP tissue. Integrated proteomic trajectories support a temporally dynamic remodeling framework linking acute inflammatory signaling to proliferative ChP activation and structural remodeling.

查看原文本刊更多论文

早产儿获得性脑积水中脉络丛重构与炎性脑脊液暴露相关。

早产儿后天性脑积水继发于脑室内出血（IVH）或中枢神经系统感染，并与脑脊液（CSF）炎症相关。我们整合了临床磁共振成像（MRI）、脑脊液细胞因子谱、原发性人脉络膜丛（ChP）上皮和内皮细胞分析以及独立的转录组学和蛋白质组学数据集来研究ChP重塑。需要脑脊液分流的婴儿表现出更大的ChP厚度，与胎龄、心室大小和IVH严重程度无关，支持其作为生物标志物的潜力。生长因子富集的炎性脑脊液增加原代人ChP上皮细胞和内皮细胞的增殖；抑制EGFR和VEGFR可减弱这些反应，重组表皮生长因子（EGF）和血管内皮生长因子（VEGF）可复制增殖效应。独立的IVH转录组学数据证实Mki67在IVH ChP组织中升高。综合蛋白质组学轨迹支持将急性炎症信号与增殖性ChP激活和结构重塑联系起来的时间动态重塑框架。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

iScience Multidisciplinary-Multidisciplinary

CiteScore

7.20

自引率

1.70%

发文量

1972

审稿时长

6 weeks

期刊介绍： Science has many big remaining questions. To address them, we will need to work collaboratively and across disciplines. The goal of iScience is to help fuel that type of interdisciplinary thinking. iScience is a new open-access journal from Cell Press that provides a platform for original research in the life, physical, and earth sciences. The primary criterion for publication in iScience is a significant contribution to a relevant field combined with robust results and underlying methodology. The advances appearing in iScience include both fundamental and applied investigations across this interdisciplinary range of topic areas. To support transparency in scientific investigation, we are happy to consider replication studies and papers that describe negative results. We know you want your work to be published quickly and to be widely visible within your community and beyond. With the strong international reputation of Cell Press behind it, publication in iScience will help your work garner the attention and recognition it merits. Like all Cell Press journals, iScience prioritizes rapid publication. Our editorial team pays special attention to high-quality author service and to efficient, clear-cut decisions based on the information available within the manuscript. iScience taps into the expertise across Cell Press journals and selected partners to inform our editorial decisions and help publish your science in a timely and seamless way.