花生四烯酸对原代人骨骼肌母细胞和肌管的剂量效应。

IF 4.5 2区 医学 Q1 NUTRITION & DIETETICS
Brandon M Roberts, Alexander L Kolb, Alyssa V Geddis, Marshall A Naimo, Ronald W Matheny
{"title":"花生四烯酸对原代人骨骼肌母细胞和肌管的剂量效应。","authors":"Brandon M Roberts,&nbsp;Alexander L Kolb,&nbsp;Alyssa V Geddis,&nbsp;Marshall A Naimo,&nbsp;Ronald W Matheny","doi":"10.1080/15502783.2022.2164209","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Cellular inflammatory response, mediated by arachidonic acid (AA) and cyclooxygenase, is a highly regulated process that leads to the repair of damaged tissue. Recent studies on murine C2C12 cells have demonstrated that AA supplementation leads to myotube hypertrophy. However, AA has not been tested on primary human muscle cells. Therefore, the purpose of this study was to determine whether AA supplementation has similar effects on human muscle cells.</p><p><strong>Methods: </strong>Proliferating and differentiating human myoblasts were exposed to AA in a dose-dependent manner (50-0.80 µM) for 48 (myoblasts) or 72 (myotubes) hours. Cell viability was tested using a 3-(4,5-Dimethylthiazol-2-Yl)-2,5-Diphenyltetrazolium Bromide (MTT) assay and cell counting; myotube area was determined by immunocytochemistry and confocal microscopy; and anabolic signaling pathways were evaluated by western blot and RT-PCR.</p><p><strong>Results: </strong>Our data show that the treatment of primary human myoblasts treated with 50 µM and 25 µM of AA led to the release of PGE<sub>2</sub> and PGF<sub>2α</sub> at levels higher than those of control-treated cells (<i>p</i> < 0.001 for all concentrations). Additionally, 50 µM and 25 µM of AA suppressed myoblast proliferation, myotube area, and myotube fusion. Anabolic signaling indicated reductions in total and phosphorylated TSC2, AKT, S6, and 4EBP1 in myoblasts at 50 µM of AA (<i>p</i> < 0.01 for all), but not in myotubes. These changes were not affected by COX-2 inhibition with celecoxib.</p><p><strong>Conclusion: </strong>Together, our data demonstrate that high concentrations of AA inhibit myoblast proliferation, myotube fusion, and myotube hypertrophy, thus revealing potential deleterious effects of AA on human skeletal muscle cell health and viability.</p>","PeriodicalId":17400,"journal":{"name":"Journal of the International Society of Sports Nutrition","volume":"20 1","pages":"2164209"},"PeriodicalIF":4.5000,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9817121/pdf/","citationCount":"3","resultStr":"{\"title\":\"The dose-response effects of arachidonic acid on primary human skeletal myoblasts and myotubes.\",\"authors\":\"Brandon M Roberts,&nbsp;Alexander L Kolb,&nbsp;Alyssa V Geddis,&nbsp;Marshall A Naimo,&nbsp;Ronald W Matheny\",\"doi\":\"10.1080/15502783.2022.2164209\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Cellular inflammatory response, mediated by arachidonic acid (AA) and cyclooxygenase, is a highly regulated process that leads to the repair of damaged tissue. Recent studies on murine C2C12 cells have demonstrated that AA supplementation leads to myotube hypertrophy. However, AA has not been tested on primary human muscle cells. Therefore, the purpose of this study was to determine whether AA supplementation has similar effects on human muscle cells.</p><p><strong>Methods: </strong>Proliferating and differentiating human myoblasts were exposed to AA in a dose-dependent manner (50-0.80 µM) for 48 (myoblasts) or 72 (myotubes) hours. Cell viability was tested using a 3-(4,5-Dimethylthiazol-2-Yl)-2,5-Diphenyltetrazolium Bromide (MTT) assay and cell counting; myotube area was determined by immunocytochemistry and confocal microscopy; and anabolic signaling pathways were evaluated by western blot and RT-PCR.</p><p><strong>Results: </strong>Our data show that the treatment of primary human myoblasts treated with 50 µM and 25 µM of AA led to the release of PGE<sub>2</sub> and PGF<sub>2α</sub> at levels higher than those of control-treated cells (<i>p</i> < 0.001 for all concentrations). Additionally, 50 µM and 25 µM of AA suppressed myoblast proliferation, myotube area, and myotube fusion. Anabolic signaling indicated reductions in total and phosphorylated TSC2, AKT, S6, and 4EBP1 in myoblasts at 50 µM of AA (<i>p</i> < 0.01 for all), but not in myotubes. These changes were not affected by COX-2 inhibition with celecoxib.</p><p><strong>Conclusion: </strong>Together, our data demonstrate that high concentrations of AA inhibit myoblast proliferation, myotube fusion, and myotube hypertrophy, thus revealing potential deleterious effects of AA on human skeletal muscle cell health and viability.</p>\",\"PeriodicalId\":17400,\"journal\":{\"name\":\"Journal of the International Society of Sports Nutrition\",\"volume\":\"20 1\",\"pages\":\"2164209\"},\"PeriodicalIF\":4.5000,\"publicationDate\":\"2023-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9817121/pdf/\",\"citationCount\":\"3\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of the International Society of Sports Nutrition\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1080/15502783.2022.2164209\",\"RegionNum\":2,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"NUTRITION & DIETETICS\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of the International Society of Sports Nutrition","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/15502783.2022.2164209","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"NUTRITION & DIETETICS","Score":null,"Total":0}
引用次数: 3

摘要

背景:由花生四烯酸(AA)和环氧合酶介导的细胞炎症反应是一个高度调控的过程,可导致受损组织的修复。最近对小鼠C2C12细胞的研究表明,补充AA可导致肌管肥大。然而,AA尚未在人类原代肌肉细胞上进行测试。因此,本研究的目的是确定补充AA是否对人体肌肉细胞有类似的影响。方法:将增殖和分化的人成肌细胞以剂量依赖性(50-0.80µM)暴露于AA中48小时(成肌细胞)或72小时(肌管)。采用3-(4,5-二甲基噻唑-2-酰基)-2,5-二苯基溴化四唑(MTT)测定法和细胞计数法检测细胞活力;采用免疫细胞化学和共聚焦显微镜测定肌管面积;western blot和RT-PCR检测合成代谢信号通路。结果:我们的数据显示,用50µM和25µM AA处理的人原代成肌细胞导致PGE2和PGF2α的释放水平高于对照处理的细胞(p p)。结论:我们的数据表明,高浓度AA抑制成肌细胞增殖、肌管融合和肌管肥大,从而揭示了AA对人骨骼肌细胞健康和活力的潜在有害影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

The dose-response effects of arachidonic acid on primary human skeletal myoblasts and myotubes.

The dose-response effects of arachidonic acid on primary human skeletal myoblasts and myotubes.

The dose-response effects of arachidonic acid on primary human skeletal myoblasts and myotubes.

The dose-response effects of arachidonic acid on primary human skeletal myoblasts and myotubes.

Background: Cellular inflammatory response, mediated by arachidonic acid (AA) and cyclooxygenase, is a highly regulated process that leads to the repair of damaged tissue. Recent studies on murine C2C12 cells have demonstrated that AA supplementation leads to myotube hypertrophy. However, AA has not been tested on primary human muscle cells. Therefore, the purpose of this study was to determine whether AA supplementation has similar effects on human muscle cells.

Methods: Proliferating and differentiating human myoblasts were exposed to AA in a dose-dependent manner (50-0.80 µM) for 48 (myoblasts) or 72 (myotubes) hours. Cell viability was tested using a 3-(4,5-Dimethylthiazol-2-Yl)-2,5-Diphenyltetrazolium Bromide (MTT) assay and cell counting; myotube area was determined by immunocytochemistry and confocal microscopy; and anabolic signaling pathways were evaluated by western blot and RT-PCR.

Results: Our data show that the treatment of primary human myoblasts treated with 50 µM and 25 µM of AA led to the release of PGE2 and PGF at levels higher than those of control-treated cells (p < 0.001 for all concentrations). Additionally, 50 µM and 25 µM of AA suppressed myoblast proliferation, myotube area, and myotube fusion. Anabolic signaling indicated reductions in total and phosphorylated TSC2, AKT, S6, and 4EBP1 in myoblasts at 50 µM of AA (p < 0.01 for all), but not in myotubes. These changes were not affected by COX-2 inhibition with celecoxib.

Conclusion: Together, our data demonstrate that high concentrations of AA inhibit myoblast proliferation, myotube fusion, and myotube hypertrophy, thus revealing potential deleterious effects of AA on human skeletal muscle cell health and viability.

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
Journal of the International Society of Sports Nutrition
Journal of the International Society of Sports Nutrition NUTRITION & DIETETICS-SPORT SCIENCES
CiteScore
8.80
自引率
3.90%
发文量
34
审稿时长
6-12 weeks
期刊介绍: Journal of the International Society of Sports Nutrition (JISSN) focuses on the acute and chronic effects of sports nutrition and supplementation strategies on body composition, physical performance and metabolism. JISSN is aimed at researchers and sport enthusiasts focused on delivering knowledge on exercise and nutrition on health, disease, rehabilitation, training, and performance. The journal provides a platform on which readers can determine nutritional strategies that may enhance exercise and/or training adaptations leading to improved health and performance.
×
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:481959085
Book学术官方微信