• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

心脏分化促进 H9c2 心肌细胞中线粒体的发育和氧化能力的改善。

Cardiac differentiation promotes mitochondria development and ameliorates oxidative capacity in H9c2 cardiomyoblasts.

机构信息

Department of Biomedical Sciences and Technologies, University of Udine, Udine, Italy.

出版信息

Mitochondrion. 2011 Mar;11(2):315-26. doi: 10.1016/j.mito.2010.12.007. Epub 2010 Dec 13.

DOI:10.1016/j.mito.2010.12.007
PMID:21147273
Abstract

H9c2 undergoing cardiac differentiation induced by all-trans-retinoic acid were investigated for mitochondria structural features together with the implied functional changes, as a model for the study of mitochondrial development in cardiogenic progenitor cells. As the expression of cardiac markers became detectable, mitochondrial mass increased and mitochondrial morphology and ultrastructure changed. Reticular network organization developed and more bulky mitochondria with greater numbers of closely packed cristae and more electron-dense matrix were detected. Increased expression of PGC-1α proved the occurrence of mitochondrial biogenesis. Improvements in mitochondrial energetic competence were also documented, linked to better assembly between F(0) and F(1) sectors of the F(0)F(1)ATPsynthase enzyme complex.

摘要

用全反式视黄酸诱导 H9c2 细胞向心肌细胞分化,研究其线粒体结构特征及潜在的功能变化,作为研究成心机细胞中线粒体发育的模型。随着心肌标志物的表达变得可检测,线粒体质量增加,线粒体形态和超微结构发生变化。网状网络组织发育,检测到具有更多紧密堆积的嵴和更密集的电子致密基质的更大体积的线粒体。PGC-1α 的表达增加证明了线粒体生物发生的发生。还记录了线粒体能量能力的改善,这与 F(0)F(1)ATP 合酶酶复合物的 F(0)和 F(1) 部分之间更好的组装有关。

相似文献

1
Cardiac differentiation promotes mitochondria development and ameliorates oxidative capacity in H9c2 cardiomyoblasts.心脏分化促进 H9c2 心肌细胞中线粒体的发育和氧化能力的改善。
Mitochondrion. 2011 Mar;11(2):315-26. doi: 10.1016/j.mito.2010.12.007. Epub 2010 Dec 13.
2
Doxorubicin-induced mitochondrial dysfunction is secondary to nuclear p53 activation in H9c2 cardiomyoblasts.阿霉素诱导的线粒体功能障碍继发于H9c2心肌母细胞中的核p53激活。
Cancer Chemother Pharmacol. 2009 Sep;64(4):811-27. doi: 10.1007/s00280-009-0932-x. Epub 2009 Jan 30.
3
Mechanical stretch induces mitochondria-dependent apoptosis in neonatal rat cardiomyocytes and G2/M accumulation in cardiac fibroblasts.机械牵张可诱导新生大鼠心肌细胞发生线粒体依赖性凋亡,并使心脏成纤维细胞发生G2/M期阻滞。
Cell Res. 2004 Feb;14(1):16-26. doi: 10.1038/sj.cr.7290198.
4
N-acetylcysteine prevents glucose/glucose oxidase-induced oxidative stress, mitochondrial damage and apoptosis in H9c2 cells.N-乙酰半胱氨酸可预防葡萄糖/葡萄糖氧化酶诱导的H9c2细胞氧化应激、线粒体损伤和细胞凋亡。
Life Sci. 2009 Mar 13;84(11-12):328-36. doi: 10.1016/j.lfs.2008.12.016. Epub 2008 Dec 31.
5
Domoic acid impairment of cardiac energetics.软骨藻酸对心脏能量代谢的损害。
Toxicol Sci. 2008 Oct;105(2):395-407. doi: 10.1093/toxsci/kfn132. Epub 2008 Jul 1.
6
Mitochondrial proliferation during apoptosis induced by anticancer agents: effects of doxorubicin and mitoxantrone on cancer and cardiac cells.抗癌药物诱导凋亡过程中的线粒体增殖:阿霉素和米托蒽醌对癌细胞和心脏细胞的影响。
Oncogene. 2004 Sep 16;23(42):7018-30. doi: 10.1038/sj.onc.1207936.
7
Attenuation of myocardial apoptosis by alpha-lipoic acid through suppression of mitochondrial oxidative stress to reduce diabetic cardiomyopathy.通过抑制线粒体氧化应激来减少糖尿病心肌病,从而减轻心肌细胞凋亡。
Chin Med J (Engl). 2009 Nov 5;122(21):2580-6.
8
Wy-14,643 and fenofibrate inhibit mitochondrial respiration in isolated rat cardiac mitochondria.Wy-14643和非诺贝特抑制离体大鼠心脏线粒体的呼吸作用。
Mitochondrion. 2006 Dec;6(6):315-22. doi: 10.1016/j.mito.2006.09.001. Epub 2006 Sep 7.
9
The Metabolic Effects of Traditional Chinese Medication Qiliqiangxin on H9C2 Cardiomyocytes.中药芪苈强心对H9C2心肌细胞的代谢作用
Cell Physiol Biochem. 2015;37(6):2246-56. doi: 10.1159/000438580. Epub 2015 Nov 29.
10
Aging selectively decreases oxidative capacity in rat heart interfibrillar mitochondria.衰老选择性地降低大鼠心脏肌原纤维间线粒体的氧化能力。
Arch Biochem Biophys. 1999 Dec 15;372(2):399-407. doi: 10.1006/abbi.1999.1508.

引用本文的文献

1
Systematic cryopreservation study of cardiac myoblasts in suspension.悬浮状态下心肌细胞的系统冷冻保存研究。
PLoS One. 2024 Mar 6;19(3):e0295131. doi: 10.1371/journal.pone.0295131. eCollection 2024.
2
Temperature Dependence of Membrane Permeability Parameters for Five Cell Types Using Nonideal Thermodynamic Assumptions to Mathematically Model Cryopreservation Protocols.基于非理想热力学假设,利用数学模型模拟冷冻保存方案,计算五种细胞类型的膜渗透参数的温度依赖性。
J Phys Chem B. 2024 Feb 8;128(5):1139-1160. doi: 10.1021/acs.jpcb.3c04534. Epub 2024 Jan 31.
3
Facile Fabrication of Three-Dimensional Hydrogel Film with Complex Tissue Morphology.
具有复杂组织形态的三维水凝胶薄膜的简易制备
Bioengineering (Basel). 2021 Oct 27;8(11):164. doi: 10.3390/bioengineering8110164.
4
HIF1α-dependent mitophagy facilitates cardiomyoblast differentiation.低氧诱导因子1α依赖性线粒体自噬促进心肌成纤维细胞分化。
Cell Stress. 2020 Mar 4;4(5):99-113. doi: 10.15698/cst2020.05.220.
5
Sustained phospholipase C stimulation of H9c2 cardiomyoblasts by vasopressin induces an increase in CDP-diacylglycerol synthase 1 (CDS1) through protein kinase C and cFos.血管加压素持续刺激 H9c2 心肌细胞可通过蛋白激酶 C 和 c-Fos 增加 CDP-二酰基甘油合成酶 1(CDS1)。
Biochim Biophys Acta Mol Cell Biol Lipids. 2019 Jul;1864(7):1072-1082. doi: 10.1016/j.bbalip.2019.03.002. Epub 2019 Mar 9.
6
Mitochondrial CDP-diacylglycerol synthase activity is due to the peripheral protein, TAMM41 and not due to the integral membrane protein, CDP-diacylglycerol synthase 1.线粒体 CDP-二酰基甘油合酶活性归因于外周蛋白 TAMM41,而不是归因于整合膜蛋白 CDP-二酰基甘油合酶 1。
Biochim Biophys Acta Mol Cell Biol Lipids. 2018 Mar;1863(3):284-298. doi: 10.1016/j.bbalip.2017.12.005. Epub 2017 Dec 16.
7
Mitochondrial energy metabolism and signalling in human glioblastoma cell lines with different PTEN gene status.具有不同 PTEN 基因状态的人胶质母细胞瘤细胞系中线粒体能量代谢和信号转导。
J Bioenerg Biomembr. 2018 Feb;50(1):33-52. doi: 10.1007/s10863-017-9737-5. Epub 2017 Dec 6.
8
Surface-modified particles loaded with CaMKII inhibitor protect cardiac cells against mitochondrial injury.负载钙调蛋白激酶II抑制剂的表面改性颗粒可保护心脏细胞免受线粒体损伤。
Int J Pharm. 2017 Mar 30;520(1-2):275-283. doi: 10.1016/j.ijpharm.2017.01.061. Epub 2017 Feb 3.
9
Tauroursodeoxycholic acid inhibits endoplasmic reticulum stress, blocks mitochondrial permeability transition pore opening, and suppresses reperfusion injury through GSK-3ß in cardiac H9c2 cells.牛磺熊去氧胆酸通过抑制心脏H9c2细胞中的内质网应激、阻止线粒体通透性转换孔开放以及抑制糖原合成酶激酶3β(GSK-3β)来减轻再灌注损伤。
Am J Transl Res. 2016 Nov 15;8(11):4586-4597. eCollection 2016.
10
Gene Expression Profiling of H9c2 Myoblast Differentiation towards a Cardiac-Like Phenotype.H9c2成肌细胞向类心脏表型分化的基因表达谱分析。
PLoS One. 2015 Jun 29;10(6):e0129303. doi: 10.1371/journal.pone.0129303. eCollection 2015.