Y chromosome–linked UTY modulates sex differences in valvular fibroblast methylation in response to nanoscale extracellular matrix cues

IF 12.5 1区 综合性期刊 Q1 MULTIDISCIPLINARY SCIENCES
Rayyan M. Gorashi, Talia Baddour, Sarah J. Chittle, Nicole E. Félix Vélez, Michaela A. Wenning, Kristi S. Anseth, Luisa Mestroni, Brisa Peña, Peng Guo, Brian A. Aguado
{"title":"Y chromosome–linked UTY modulates sex differences in valvular fibroblast methylation in response to nanoscale extracellular matrix cues","authors":"Rayyan M. Gorashi, Talia Baddour, Sarah J. Chittle, Nicole E. Félix Vélez, Michaela A. Wenning, Kristi S. Anseth, Luisa Mestroni, Brisa Peña, Peng Guo, Brian A. Aguado","doi":"10.1126/sciadv.ads5717","DOIUrl":null,"url":null,"abstract":"Aortic valve stenosis (AVS) is a progressive disease, wherein males more often develop valve calcification relative to females that develop valve fibrosis. Valvular interstitial cells (VICs) aberrantly activate to myofibroblasts during AVS, driving the fibrotic valve phenotype in females. Myofibroblasts further differentiate into osteoblast-like cells and produce calcium nanoparticles, driving valve calcification in males. We hypothesized that the lysine demethylase UTY (ubiquitously transcribed tetratricopeptide repeat containing Y-linked) decreases methylation uniquely in male VICs responding to nanoscale extracellular matrix cues to promote an osteoblast-like cell phenotype. Here, we describe a hydrogel biomaterial cell culture platform to interrogate how nanoscale cues modulate sex-specific methylation states in VICs activating to myofibroblasts and osteoblast-like cells. We found that UTY modulates the osteoblast-like cell phenotype in response to nanoscale cues uniquely in male VICs. Overall, we reveal a previously unidentified role of UTY in the regulation of calcification processes in males during AVS progression.","PeriodicalId":21609,"journal":{"name":"Science Advances","volume":"54 1","pages":""},"PeriodicalIF":12.5000,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Science Advances","FirstCategoryId":"103","ListUrlMain":"https://doi.org/10.1126/sciadv.ads5717","RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"MULTIDISCIPLINARY SCIENCES","Score":null,"Total":0}
引用次数: 0

Abstract

Aortic valve stenosis (AVS) is a progressive disease, wherein males more often develop valve calcification relative to females that develop valve fibrosis. Valvular interstitial cells (VICs) aberrantly activate to myofibroblasts during AVS, driving the fibrotic valve phenotype in females. Myofibroblasts further differentiate into osteoblast-like cells and produce calcium nanoparticles, driving valve calcification in males. We hypothesized that the lysine demethylase UTY (ubiquitously transcribed tetratricopeptide repeat containing Y-linked) decreases methylation uniquely in male VICs responding to nanoscale extracellular matrix cues to promote an osteoblast-like cell phenotype. Here, we describe a hydrogel biomaterial cell culture platform to interrogate how nanoscale cues modulate sex-specific methylation states in VICs activating to myofibroblasts and osteoblast-like cells. We found that UTY modulates the osteoblast-like cell phenotype in response to nanoscale cues uniquely in male VICs. Overall, we reveal a previously unidentified role of UTY in the regulation of calcification processes in males during AVS progression.
Y 染色体连锁UTY调节瓣膜成纤维细胞甲基化的性别差异,以响应纳米级细胞外基质线索
主动脉瓣狭窄(AVS)是一种进行性疾病,其中男性更常发生瓣膜钙化,而女性更常发生瓣膜纤维化。瓣膜间质细胞(VICs)在AVS期间异常激活为肌成纤维细胞,驱动女性纤维化瓣膜表型。肌成纤维细胞进一步分化为成骨细胞样细胞并产生钙纳米颗粒,驱动男性瓣膜钙化。我们假设赖氨酸去甲基化酶UTY(含y链的普遍转录的四肽重复序列)在男性VICs中对纳米级细胞外基质线索做出反应,从而促进成骨细胞样细胞表型,从而独特地降低甲基化。在这里,我们描述了一个水凝胶生物材料细胞培养平台,以询问纳米尺度线索如何调节VICs激活到肌成纤维细胞和成骨细胞样细胞中的性别特异性甲基化状态。我们发现UTY调节成骨细胞样细胞表型,以响应纳米尺度的线索,这在男性vic中是独一无二的。总的来说,我们揭示了UTY在AVS进展过程中对男性钙化过程的调节中的先前未确定的作用。
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
Science Advances
Science Advances 综合性期刊-综合性期刊
CiteScore
21.40
自引率
1.50%
发文量
1937
审稿时长
29 weeks
期刊介绍: Science Advances, an open-access journal by AAAS, publishes impactful research in diverse scientific areas. It aims for fair, fast, and expert peer review, providing freely accessible research to readers. Led by distinguished scientists, the journal supports AAAS's mission by extending Science magazine's capacity to identify and promote significant advances. Evolving digital publishing technologies play a crucial role in advancing AAAS's global mission for science communication and benefitting humankind.
×
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