Small Amounts of &agr;-Myosin Heavy Chain Isoform Expression Significantly Increase Power Output of Rat Cardiac Myocyte Fragments

T. Herron, K. McDonald
{"title":"Small Amounts of &agr;-Myosin Heavy Chain Isoform Expression Significantly Increase Power Output of Rat Cardiac Myocyte Fragments","authors":"T. Herron, K. McDonald","doi":"10.1161/01.RES.0000022879.57270.11","DOIUrl":null,"url":null,"abstract":"Myocardial performance is likely affected by the relative expression of the two myosin heavy chain (MyHC) isoforms, namely &agr;-MyHC and &bgr;-MyHC. The relative expression of each isoform is regulated developmentally and in pathophysiological states. Many pathophysiological states are associated with small shifts in the relative expression of each MyHC isoform, yet the functional consequence of these shifts remains unclear. The purpose of this study was to determine the functional effect of a small shift in the relative expression of &agr;-MyHC. To this end, power output was measured in rat cardiac myocyte fragments that expressed ≈12% &agr;-MyHC and in myocyte fragments that expressed ≈0% &agr;-MyHC, as determined in the same cells by SDS-PAGE analysis after mechanical experiments. Myocyte fragments expressing ≈12% &agr;-MyHC developed ≈52% greater peak normalized power output than myocyte fragments expressing ≈0% &agr;-MyHC. These results indicate that small amounts of &agr;-MyHC expression significantly augment myocyte power output.","PeriodicalId":10314,"journal":{"name":"Circulation Research: Journal of the American Heart Association","volume":"89 12 1","pages":"1150-1152"},"PeriodicalIF":0.0000,"publicationDate":"2002-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"218","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Circulation Research: Journal of the American Heart Association","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1161/01.RES.0000022879.57270.11","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 218

Abstract

Myocardial performance is likely affected by the relative expression of the two myosin heavy chain (MyHC) isoforms, namely &agr;-MyHC and &bgr;-MyHC. The relative expression of each isoform is regulated developmentally and in pathophysiological states. Many pathophysiological states are associated with small shifts in the relative expression of each MyHC isoform, yet the functional consequence of these shifts remains unclear. The purpose of this study was to determine the functional effect of a small shift in the relative expression of &agr;-MyHC. To this end, power output was measured in rat cardiac myocyte fragments that expressed ≈12% &agr;-MyHC and in myocyte fragments that expressed ≈0% &agr;-MyHC, as determined in the same cells by SDS-PAGE analysis after mechanical experiments. Myocyte fragments expressing ≈12% &agr;-MyHC developed ≈52% greater peak normalized power output than myocyte fragments expressing ≈0% &agr;-MyHC. These results indicate that small amounts of &agr;-MyHC expression significantly augment myocyte power output.
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
少量的&agr;-肌球蛋白重链异构体表达可显著增加大鼠心肌细胞片段的能量输出
心肌表现可能受到两种肌球蛋白重链(MyHC)亚型,即&agr;-MyHC和&bgr;-MyHC的相对表达的影响。每个亚型的相对表达在发育和病理生理状态下受到调节。许多病理生理状态与每种MyHC亚型相对表达的微小变化有关,但这些变化的功能后果尚不清楚。本研究的目的是确定&agr;-MyHC相对表达的微小变化对功能的影响。为此,我们测量了表达≈12% &agr;-MyHC的大鼠心肌细胞片段和表达≈0% &agr;-MyHC的心肌细胞片段的输出功率,在机械实验后通过SDS-PAGE分析确定了相同细胞的输出功率。表达≈12% &agr;-MyHC的肌细胞片段比表达≈0% &agr;-MyHC的肌细胞片段的峰值归一化功率输出高约52%。这些结果表明,少量的&agr;-MyHC表达显著增加了肌细胞的能量输出。
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 去求助
来源期刊
自引率
0.00%
发文量
0
期刊最新文献
Neuron-Derived Orphan Receptor-1 (NOR-1) Modulates Vascular Smooth Muscle Cell Proliferation Functional Compartmentation of Endothelial P2Y Receptor Signaling Cardiac Microstructure: Implications for Electrical Propagation and Defibrillation in the Heart Increased Exchange Current but Normal Ca2+ Transport via Na+-Ca2+ Exchange During Cardiac Hypertrophy After Myocardial Infarction Functionally Novel Tumor Necrosis Factor-&agr;–Modulated CHR-Binding Protein Mediates Cyclin A Transcriptional Repression in Vascular Endothelial Cells
×
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
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 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 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1