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10篇 您的检索式:作者名="Neal WEINTRAUB"
    题名 作者 年代 出处 被引量
1Exosomes from Suxiao Jiuxin pill-treated cardiac mesenchymal stem cells decrease H3K27 demethylase UTX expression in mouse cardiomyocytes in vitro显示文摘Suxiao Jiuxin 药片(SJP ) 是为在中国的急性冠的症候群的处理的繁体中文药,它包含二个主要部件, tetramethylpyrazine (TMP ) 和龙脑(BOR ) 。因此远然而,在心脏的微型环境上位于 SJP 的有益的效果下面的分子的机制是未知的。心脏的间充质的干细胞(C-MSCs ) 通过 microvesicles (exosomes ) 的版本与 cardiomyocytes (厘米) 交流恢复心脏的动态平衡并且得到修理,部分地通过 epigenetic 规章的机制。在这研究,我们检验了 SJP 处理是否改变了 C-MSC-derived exosomes (SJP-Exos ) 引起 epigenetic 在接受者厘米的色彩的改变。从老鼠心孤立的 C-MSC 是有 SJP (SJP-Exos ) 的 pretreated, TMP (TMP-Exos ) 或 BOR (BOR-Exos ) 。然后, HL-1 房间,一根鼠标 cardiomyocyte 线,从控制与 exosomes 被对待 C-MSCs (Ctrl-Exos ) , SJP-Exos, TMP-Exos 或 BOR-Exos。有 SJP-Exos 的处理显著地增加了 histone 的蛋白质层次 3 离氨酸 27 trimethylation (H3K27me3 ) ,为心脏的 transcriptional 抑制的一个关键 epigenetic 染色质标记,在 HL-1 房间。为了推进,探索 SJP-Exo-mediated H3K27me3 upregulation 的机制,我们在对待 exosome 的 HL-1 房间估计了关键 histone methylases (EZH1, EZH2 和 EED ) 和 demethylases (JMJD3 和 UTX ) 的 mRNA 表示层次。有 SJP-Exo 的处理有选择地在接受者 HL-1 房间压制了 UTX 表示。而且, PCNA,房间复制的一个内长的标记,比在 Ctrl-Exo-treated HL-1 房间在 SJP-Exo-treated HL-1 房间是显著地更高的。这些结果证明 SJP-Exos 增加 cardiomyocyte 增长并且证明 SJP 能调制 C-MSC-derived exosomes 引起 epigenetic 染色质在接受者 cardiomyocytes 改变;因而, SJP-Exos 可能被用来支持 cardiomyocyte 增长。Xiao-fen RUAN Yongdun LI Cheng-wei JU Yan SHEN Wei LEI Can CHEN Yang LI Hong YU Yu-tao LIU II-man KIM Xiao-long WANG Neal L WEINTRAUB Yaoliang TANG 2018Acta Pharmacologica Sinica2018,39,4:23
2Suxiao Jiuxin pill promotes exosome secretion from mouse cardiac mesenchymal stem cells in vitro显示文摘心脏的间充质的干细胞(C-MSCs ) 是在损害以后在心修理起一个作用的内长的心脏的 stromal 房间。C-MSC-derived exosomes (Exo ) 对尖锐心肌的 ischemia/reperfusion 导致的 apoptosis 显示出保护的效果。Suxiao Jiuxin 药片(SJP ) 是为尖锐心肌的局部缺血的处理在中国使用的一个繁体中文药(TCM ) 公式,它作为主要部件包含 tetramethylpyrazine (TMP ) 和龙脑(BOR ) 。在这研究,我们调查了 SJP 处理是否在 vitro 从 C-MSCs 影响了 exosome 版本。从老鼠准备的 C-MSCs 与 SJP (62.5 g/mL ) 被对待, TMP (25 g/mL ) 或 BOR (15 g/mL ) 。用 acetylcholinesterase 活动试金,我们发现 SJP 和 TMP 处理显著地与控制乙醇处理相比增加了 exosome 分泌物。中立 sphingomyelinase 2 (nSMase2 ) 小径在 exosome 形成是重要的并且包装。但是 nSMase2 mRNA 的既不水平也不蛋白质的水平改变了后面的 SJP, TMP 或 BOR 处理,建议那 SJP 经由一条 nSMase2 独立的小径刺激了 exosome 版本。Rab27a 和 Rab27b GTPases 控制了 exosome 分泌物小径的不同步骤。我们证明 SJP 处理显著地与控制处理相比增加了 Rab27a, SYTL4 (Rab27a 受动器) 和 Rab27b 的蛋白质层次。SJP 处理另外显著地 upregulated Rab27b 的 mRNA 水平,而非 Rab27a。而且, C-MSC-exosome 版本的导致 SJP 的增加被 Rab27b 禁止击倒,建议那 SJP 经由一条 GTPase 依赖的小径从 C-MSCs 支持 exosome 分泌物。这研究在 modulating 为 SJP 揭示新奇机制心脏的动态平衡。Xiao-fen RUAN Cheng-wei JU Yan SHEN Yu-tao LIU II-man KIM Hong YU Neal WEINTRAUB Xiao-long WANG Yaoliang TANG 2018Acta Pharmacologica Sinica2018,39,4:19
3Novel concepts in radiation-induced cardiovascular disease显示文摘Radiation-induced cardiovascular disease(RICVD) is the most common nonmalignant cause of morbidity and mortality among cancer survivors who have undergone mediastinal radiation therapy(RT).Cardiovascular complications include effusive or constrictive pericarditis,cardiomyopathy,valvular heart disease,and coronary/vascular disease.These are pathophysiologically distinct disease entities whose prevalence varies depending on the timing and extent of radiation exposure to the heart and great vessels.Although refinements in RT dosimetry and shielding will inevitably limit future cases of RICVD,the increasing number of long-term cancer survivors,including those treated with older higher-dose RT regimens,will ensure a steady flow of afflicted patients for the foreseeable future.Thus,there is a pressing need for enhanced understanding of the disease mechanisms,and improved detection methods and treatment strategies.Newly characterized mechanisms responsible for the establishment of chronic fibrosis,such as oxidative stress,inflammation and epigenetic modifications,are discussed and linked to potential treatments currently under study.Novel imaging modalities may serve as powerful screening tools in RICVD,and recent research and expert opinion advocating their use is introduced.Data arguing for the aggressive use of percutaneous interventions,such as transcutaneous valve replacement and drug-eluting stents,are examined and considered in the context of prior therapeutic approaches.RICVD and its treatment options are the subject of a rich and dynamic body of research,and patients who are at risk or suffering from this disease will benefit from the care of physicians with specialty expertise in the emerging field of cardiooncology.Jason R Cuomo Gyanendra K Sharma Preston D Conger Neal L Weintraub 2016World Journal of Cardiology2016,8,9:17
4Acute Heart Failure Syndromes: Emergency Department Presentation, Treatment, and Disposition: Current Approaches and Future Aims: A Scientific Statement From the American Heart Association显示文摘Neal L. Weintraub Sean P. Collins Peter S. Pang Phillip D. Levy Allen S. Anderson Cynthia Arslanian-Engoren W. Brian Gibler James K. McCord Mark B. Parshall Gary S. Francis Mihai Gheorghiade 2010Circulation2010,,:1
5Potential role of endotoxin as a proinflammatory mediator of atherosclerosis 显示文摘Lynn L Stoll Gerene M Denning Neal L Weintraub 2004Arterioscler Thromb Vase Biol2004,24,:1
6Peer evaluations of the competence of children vulnerable to psychopathology显示文摘Weintraub S Prinz RJ Neale JM 1978J Abnorm Child Psychol1978,6,4:1
7Cardiac progenitor-derived exosomes protect ischemic myocardium from acute ischemia/reperfusion injury显示文摘Lijuan Chen Yingjie Wang Yaohua Pan Lan Zhang Chengxing Shen Gangjian Qin Muhammad Ashraf Neal Weintraub Genshan Ma Yaoliang Tang 2013Biochemical and Biophysical Research Communications2013,,3:1
8Understanding Radiation-Induced Vascular Disease ? ? Editorials published in the Journal of the American College of Cardiology reflect the views of the authors and do not necessarily represent the views of JACC or the American College of Cardiology.显示文摘Neal L. Weintraub W. Keith Jones David Manka 2010Journal of the American College of Cardiology2010,,12:1
9Epoxyeicosatrienoic acids increase intracellular calcium concentration in vascular smooth muscle cells显示文摘 Neal LW Weintraub LS 1999Hypertens1999,34,:1
10Identification of critical molecular pathways involved in exosome-mediated improvement of cardiac function in a mouse model of muscular dystrophy显示文摘Duchenne muscular dystrophy(DMD)is a progressive disease characterized by skeletal muscle atrophy,respiratory failure,and cardiomyopathy.Our previous studies have shown that transplantation with allogeneic myogenic progenitor-derived exosomes(MPC-Exo)can improve cardiac function in X-linked muscular dystrophy(Mdx)mice.In the present study we explored the molecular mechanisms underlying this beneficial effect.We quantified gene expression in the hearts of two strains of Mdx mice(D2.B10-Dmd^(Mdx)/J and Utrn^(tm1Ked)-Dmd^(Mdx)/J).Two days after MPC-Exo or control treatment,we performed unbiased next-generation RNA-sequencing to identify differentially expressed genes(DEGs)in treated Mdx hearts.Venn diagrams show a set of 780 genes that were≥2-fold upregulated,and a set of 878 genes that were≥2-fold downregulated,in both Mdx strains following MPC-Exo treatment as compared with control.Gene ontology(GO)and protein-protein interaction(PPI)network analysis showed that these DEGs were involved in a variety of physiological processes and pathways with a complex connection.qRT-PCR was performed to verify the upregulated ATP2B4 and Bcl-2 expression,and downregulated IL-6,MAPK8 and Wnt5a expression in MPC-Exo-treated Mdx hearts.Western blot analysis verified the increased level of Bcl-2 and decreased level of IL-6 protein in MPC-Exo-treated Mdx hearts compared with control treatment,suggesting that anti-apoptotic and anti-inflammatory effects might be responsible for heart function improvement by MPC-Exo.Based on these findings,we believed that these DEGs might be therapeutic targets that can be explored to develop new strategies for treating DMD.Xuan Su Yan Shen Yue Jin Neal L Weintraub Yao-liang Tang 2021Acta Pharmacologica Sinica2021,42,4:0
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