FNDC5减轻ApoE-/-小鼠动脉粥样硬化斑块的形成并调节PPARα/HO-1。

IF 1.8 4区 医学 Q3 PERIPHERAL VASCULAR DISEASE Journal of Vascular Research Pub Date : 2023-01-01 Epub Date: 2023-08-16 DOI:10.1159/000531585
Bo Zhou, Xiang Wang, Yao Wang, Danan Liu
{"title":"FNDC5减轻ApoE-/-小鼠动脉粥样硬化斑块的形成并调节PPARα/HO-1。","authors":"Bo Zhou,&nbsp;Xiang Wang,&nbsp;Yao Wang,&nbsp;Danan Liu","doi":"10.1159/000531585","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>This study attempted to observe the role of fibronectin type III domain-containing protein 5 (FNDC5) in atherosclerosis development and the underlying mechanism.</p><p><strong>Methods: </strong>After being fed a high-fat diet (HFD), ApoE-/- mice were injected with saline, control adenovirus (Ad-vector), or FNDC5 overexpressing adenovirus (Ad-FNDC5). ApoE-/- mice fed with a chow diet were considered the control. After 12 weeks of treatment, the levels of serum high-density lipoprotein cholesterol (HDL-C), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), triglyceride (TG), and irisin were detected by commercial kits.</p><p><strong>Results: </strong>Compared with the control, the serum TG, TC, and LDL-C levels, aortic plaque area, and weight were significantly increased, while serum HDL-C and irisin levels were reduced in HFD mice. Treating with Ad-FNDC5 could alleviate these changes in HFD mice and cause the activation of PPARα/HO-1 signaling in aortic tissue. After co-treating with GW6471, a PPARα antagonist, the effects of Ad-FNDC5 on the weight, serum LDL-C, TC, TG, and HDL-C levels, and aortic plaque of HFD mice were partly blocked.</p><p><strong>Conclusion: </strong>Elevated FNDC5 has a delaying effect on atherosclerotic plaque formation, which may be related to the upregulation of PPARα/HO-1 signaling.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"172-182"},"PeriodicalIF":1.8000,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":"{\"title\":\"FNDC5 Attenuates Atherosclerotic Plaque Formation and Regulates PPARα/HO-1 in ApoE-/- Mice.\",\"authors\":\"Bo Zhou,&nbsp;Xiang Wang,&nbsp;Yao Wang,&nbsp;Danan Liu\",\"doi\":\"10.1159/000531585\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Introduction: </strong>This study attempted to observe the role of fibronectin type III domain-containing protein 5 (FNDC5) in atherosclerosis development and the underlying mechanism.</p><p><strong>Methods: </strong>After being fed a high-fat diet (HFD), ApoE-/- mice were injected with saline, control adenovirus (Ad-vector), or FNDC5 overexpressing adenovirus (Ad-FNDC5). ApoE-/- mice fed with a chow diet were considered the control. After 12 weeks of treatment, the levels of serum high-density lipoprotein cholesterol (HDL-C), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), triglyceride (TG), and irisin were detected by commercial kits.</p><p><strong>Results: </strong>Compared with the control, the serum TG, TC, and LDL-C levels, aortic plaque area, and weight were significantly increased, while serum HDL-C and irisin levels were reduced in HFD mice. Treating with Ad-FNDC5 could alleviate these changes in HFD mice and cause the activation of PPARα/HO-1 signaling in aortic tissue. After co-treating with GW6471, a PPARα antagonist, the effects of Ad-FNDC5 on the weight, serum LDL-C, TC, TG, and HDL-C levels, and aortic plaque of HFD mice were partly blocked.</p><p><strong>Conclusion: </strong>Elevated FNDC5 has a delaying effect on atherosclerotic plaque formation, which may be related to the upregulation of PPARα/HO-1 signaling.</p>\",\"PeriodicalId\":17530,\"journal\":{\"name\":\"Journal of Vascular Research\",\"volume\":\" \",\"pages\":\"172-182\"},\"PeriodicalIF\":1.8000,\"publicationDate\":\"2023-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"1\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Vascular Research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1159/000531585\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2023/8/16 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q3\",\"JCRName\":\"PERIPHERAL VASCULAR DISEASE\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Vascular Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1159/000531585","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2023/8/16 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"PERIPHERAL VASCULAR DISEASE","Score":null,"Total":0}
引用次数: 1

摘要

引言:本研究试图观察含有纤连蛋白III结构域的蛋白5(FNDC5)在动脉粥样硬化发展中的作用及其潜在机制。方法:在喂食高脂饮食(HFD)后,ApoE-/-小鼠注射生理盐水、对照腺病毒(Ad载体)或FNDC5过表达腺病毒(Ad-FNDC5)。喂食日粮的ApoE-/-小鼠被认为是对照。治疗12周后,通过商业试剂盒检测血清高密度脂蛋白胆固醇(HDL-C)、总胆固醇(TC)、低密度脂蛋白胆甾醇(LDL-C)、甘油三酯(TG)和鸢尾素的水平。结果:与对照组相比,HFD小鼠血清TG、TC和LDL-C水平、主动脉斑块面积和体重显著增加,而血清HDL-C和鸢尾素水平降低。用Ad-FNDC5治疗可以减轻HFD小鼠的这些变化,并引起主动脉组织PPARα/HO-1信号的激活。在与PPARα拮抗剂GW6471共同治疗后,Ad-FNDC5对HFD小鼠体重、血清LDL-C、TC、TG和HDL-C水平以及主动脉斑块的影响被部分阻断。结论:FNDC5升高对动脉粥样硬化斑块形成具有延缓作用,可能与PPARα/HO-1信号的上调有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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
FNDC5 Attenuates Atherosclerotic Plaque Formation and Regulates PPARα/HO-1 in ApoE-/- Mice.

Introduction: This study attempted to observe the role of fibronectin type III domain-containing protein 5 (FNDC5) in atherosclerosis development and the underlying mechanism.

Methods: After being fed a high-fat diet (HFD), ApoE-/- mice were injected with saline, control adenovirus (Ad-vector), or FNDC5 overexpressing adenovirus (Ad-FNDC5). ApoE-/- mice fed with a chow diet were considered the control. After 12 weeks of treatment, the levels of serum high-density lipoprotein cholesterol (HDL-C), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), triglyceride (TG), and irisin were detected by commercial kits.

Results: Compared with the control, the serum TG, TC, and LDL-C levels, aortic plaque area, and weight were significantly increased, while serum HDL-C and irisin levels were reduced in HFD mice. Treating with Ad-FNDC5 could alleviate these changes in HFD mice and cause the activation of PPARα/HO-1 signaling in aortic tissue. After co-treating with GW6471, a PPARα antagonist, the effects of Ad-FNDC5 on the weight, serum LDL-C, TC, TG, and HDL-C levels, and aortic plaque of HFD mice were partly blocked.

Conclusion: Elevated FNDC5 has a delaying effect on atherosclerotic plaque formation, which may be related to the upregulation of PPARα/HO-1 signaling.

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 Vascular Research
Journal of Vascular Research 医学-生理学
CiteScore
3.40
自引率
0.00%
发文量
25
审稿时长
>12 weeks
期刊介绍: The ''Journal of Vascular Research'' publishes original articles and reviews of scientific excellence in vascular and microvascular biology, physiology and pathophysiology. The scope of the journal covers a broad spectrum of vascular and lymphatic research, including vascular structure, vascular function, haemodynamics, mechanics, cell signalling, intercellular communication, growth and differentiation. JVR''s ''Vascular Update'' series regularly presents state-of-the-art reviews on hot topics in vascular biology. Manuscript processing times are, consistent with stringent review, kept as short as possible due to electronic submission. All articles are published online first, ensuring rapid publication. The ''Journal of Vascular Research'' is the official journal of the European Society for Microcirculation. A biennial prize is awarded to the authors of the best paper published in the journal over the previous two years, thus encouraging young scientists working in the exciting field of vascular biology to publish their findings.
期刊最新文献
RIP3 augments neuroinflammation by facilitating neutrophil infiltration during an ischemic stroke. Characterising the Time Course of the Dilatory Response of Healthy Retinal Arteries during Flicker-Light Provocation. Perfusion staining methods for visualization of the intact microvascular networks in whole mount skeletal muscle preparations. Cerebral Cortical Vasodilation via Nicotinic Receptors by Heated Tobacco Product Aerosol Extract in Rats. Rivaroxaban as a protector of Oxidative Stress-induced Vascular Endothelial Glycocalyx Damage via The IQGAP1/PAR1-2/PI3K/Akt Pathway.
×
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