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| 1 | Mouse macrophage specific knockout of SIRT1 influences macrophage polarization and promotes angiotensin Ⅱ-induced abdominal aortic aneurysm formation显示文摘Abdominal aortic aneurysm(AAA) is a vascular degenerative disease. Macrophage polarization and the balance between classically activated macrophages(M1) and alternatively activated macrophages(M2)are crucial for AAA pathogenesis. The present study aims to investigate the roles of macrophage SIRT1 in AAA formation and macrophage polarization. We found that in mouse peritoneal macrophages, SIRT1 expression was decreased after M1 stimulation, but was enhanced after M2 stimulation. Results from SIRT1^(flox/flox) mice and macrophage specific SIRT1 knockout mice with treatment of angiotensin II(Ang II)for 4 weeks showed that macrophage specific deficiency of SIRT1 increased the incidence of AAA and exacerbated the severity, including more severe aneurysm types, enlarged diameter of the aneurysm and increased degradation of elastin. In mouse aortas, SIRT1 deficiency increased the proinflammatory M1 molecule inducible nitric oxide synthase(i NOS), and decreased M2 molecules such as arginase 1(Arg1) and mannose receptor(MR). Furthermore, in peritoneal macrophages, SIRT1 deficiency increased the expression of M1 inflammatory molecules, but decreased the expression of M2 molecules. Overexpression of SIRT1 had the opposite effects. Thus, macrophage specific knockout of SIRT1 influences macrophage polarization and accelerates Ang II-induced AAA formation. | Zhuqin Zhang Jing Xu Yue Liu Tingting Wang Jianfei Pei Liqin Cheng Delong Hao Xiang Zhao Hou-Zao Chen De-Pei Liu | 2018 | Journal of Genetics and Genomics2018,45,1: | 15 |
| 2 | Endothelium-specific SIRT1 overexpression inhibits hyperglycemia-induced upregulation of vascular cell senescence显示文摘The rapidly increasing prevalence of diabetes mellitus worldwide is one of the most serious and challenging health problems in the 21st century.Mammalian sirtuin 1(SIRT1) has been shown to decrease high-glucose-induced endothelial cell senescence in vitro and prevent hyperglycemia-induced vascular dysfunction.However,a role for SIRT1 in prevention of hyperglycemia-induced vascular cell senescence in vivo remains unclear.We used endothelium-specific SIRT1 transgenic(SIRT1-Tg) mice and wild-type(WT) mice to construct a 40-week streptozotocin(STZ)-induced diabetic mouse model.In this mode,42.9% of wild-type(WT) mice and 38.5% of SIRT1-Tg mice were successfully established as diabetic.Forty weeks of hyperglycemia induced significant vascular cell senescence in aortas of mice,as indicated by upregulation of expression of senescence-associated markers including p53,p21 and plasminogen activator inhibitor-1(PAI-1).However,SIRT1-Tg diabetic mice displayed dramatically decreased expression of p53,p21 and PAI-1 compared with diabetic WT mice.Moreover,manganese superoxide dismutase expression(MnSOD) was significantly downregulated in the aortas of diabetic WT mice,but was preserved in diabetic SIRT1-Tg mice.Furthermore,expression of the oxidative stress adaptor p66Shc was significantly decreased in aortas of SIRT1-Tg diabetic mice compared with WT diabetic mice.Overall,these findings suggest that SIRT1-mediated inhibition of hyperglycemia-induced vascular cell senescence is mediated at least partly through the reduction of oxidative stress. | CHEN HouZao WAN YanZhen ZHOU Shuang LU YunBiao ZHANG ZhuQin ZHANG Ran CHEN Feng HAO DeLong ZHAO Xiang GUO ZhiChen LIU DePei LIANG ChihChuan | 2012 | Science China(Life Sciences)2012,55,6: | 14 |
| 3 | SIRT1 suppresses PMA and ionomycin-induced ICAM-1 expression in endothelial cells显示文摘Intercellular adhesion molecule-1 (ICAM-1) plays an important role in the recruitment of leukocytes to the endothelium, which causes inflammation and initiation of atherosclerosis. We have previously shown that endothelium-specific over-expression of class III deacetylase SIRT1 decreases atherosclerosis. We therefore addressed the hypothesis that SIRT1 suppresses ICAM-1 expression in the endothelial cells. Here, we found that expression of SIRT1 and ICAM-1 was significantly induced by PMA and ionomycin (PMA/Io) in human umbilical vein endothelial cells (HUVECs). Adenovirus-mediated over-expression of SIRT1 significantly inhibited PMA/Io-induced ICAM-1 expression in HUVECs. Knockdown of SIRT1 by RNA interference (RNAi) resulted in increased expression of ICAM-1 in HUVECs. Luciferase report assay showed that over-expression of SIRT1 suppressed ICAM-1 promoter activity both in basic and in PMA/Io-induced conditions. We further found that SIRT1 was involved in transcription complex binding on the ICAM-1 promoter by chromatin immunoprecipitation (ChIP) assays. Furthermore, SIRT1 RNAi increased NF-κB p65 binding ability to the ICAM-1 promoter by ChIP assays. Overall, these data suggests that SIRT1 inhibits ICAM-1 expression in endothelial cells, which may contribute to its anti-atherosclerosis effect. | JIA YuYan GAO Peng CHEN HouZao WAN YanZhen ZHANG Ran ZHANG ZhuQin YANG RuiFeng WANG Xu XU Jing LIU DePei | 2013 | Science China(Life Sciences)2013,56,1: | 9 |
| 4 | Translational research:Lessons from past research,growing up nowadays,and development goal in future显示文摘Recently,with coming of the 'omics' era and rapid development of basic research in biology and medicine,huge information about biology and life has been achieved. However,many research results cannot be translated into clinical practice. Under this circumstance,the concept | ZHANG ZhuQin CHEN HouZao LIU DePei | 2011 | Science China(Life Sciences)2011,54,12: | 7 |
| 5 | Vascular Transcriptome Profiling Reveals Aging-Related Genes in Angiotensin Ji-Induced Hypertensive Mouse Aortas显示文摘Objective AngiotensinⅡ(AngⅡ)-induced vascular damage is a major risk of hypertension.However,the underlying molecular mechanism of AngⅡ-induced vascular damage is still unclear.In this study,we explored the novel mechanism associated with Ang Il-induced hypertension.Methods We treated 8-to 12-week-old C57BL/6J male mice with saline and AngⅡ(0.72 mg/kg-d)for 28 days,respectively.Then the RNA of the media from the collected mice aortas was extracted for transcriptome sequencing.Principal component analysis was applied to show a clear separation of different samples and the distribution of differentially expressed genes was manifested by Volcano plot.Functional annotations including Gene Ontology(GO)and Koto Encyclopedia of Genes and Genomes(KEGG)pathway were performed to reveal the molecular mechanism of AngⅡ-induced hypertension.Finally,the differentially expressed genes were validated by using quantitative real-time PCR.Results The result revealed that a total of 773 genes,including 599 up-regulated genes and 174 down-regulated genes,were differentially expressed in the aorta of AngⅡ-induced hypertension mice model.Functional analysis of differentially expressed genes manifested that various cellular processes may be involved in the AngⅡ-induced hypertension,including some pathways associated with hypertension such as extracellular matrix,inflammation and immune response.Interestingly,we also found that the differentially expressed genes were enriched in vascular aging pathway,and further validated that the expression levels of insulin-like growth factor 1 and adiponectin were significantly increased(P<0.05).Conclusion We identify that vascular aging is involved in AngⅡ-induced hypertension,and insulin-like growth factor 1 and adiponectin may be important candidate genes leading to vascular aging. | Shuangjie Lv Yangnan Ding Xiaoya Pei Xiang Zhao Delong Hao Zhuqin Zhang Houzao Chen Depei Liu | 2020 | Chinese Medical Sciences Journal2020,35,1: | 4 |
| 6 | Circulating microRNA-1 as a potential novel biomarker for acute myocardial infarction显示文摘 | Jing Ai Rong Zhang Yue Li Jielin Pu Yanjie Lu Jundong Jiao Kang Li Bo Yu Zhuqin Li Rongrong Wang Lihong Wang Qiang Li Ning Wang Hongli Shan Zhongyu Li Baofeng Yang | 2009 | Biochemical and Biophysical Research Communications2009,,: | 2 |
| 7 | Two novel cis-elements involved in hepatocyte nuclear factor 4α regulation of acyl-coenzyme A:cholesterol acyltransferase 2 expression显示文摘酰辅酶 A:cholesterol acyltransferase (ACAT2 ) 2 为胆固醇酉旨合成和分泌物是重要的。以前的研究表明那项 ACAT2 基因倡导者活动是由 hepatocyte 的 upregulated 原子因素 4 (HNF4 ) 通过在 247 ACAT2 和 311 基因倡导者附近的二个地点。这里,我们识别了二新奇 cis 元素,地点我(1006 ~ 898 ) 并且地点 II (38 ~ 29 ) ,它为 HNF4 是重要的效果。在 HepG2 房间,地点的变化我减少了 ACAT2 基因倡导者活动到野类型的中的五分之一个个,当地点 II 的变化把倡导者活动归结为野类型的不到十分之一时。在 293T 房间,这二 cis 元素的变化深刻地损害了 HNF4 正式就职效果。当这二个元素的任何一个被插入到 pGL3 倡导者时, HNF4 通过插入的元素导致了倡导者活动,当元素的变化损害了 HNF4 正式就职效果时。在 electrophoretic 活动性移动试金和染色质 immunoprecipitation 实验, HNF4 跳了到这二个元素。因此,二 cis 元素为 ACAT2 基因抄写上的 HNF4 效果是重要的。我们也证明 HNF4 断然在 mRNA 水平调整 ACAT2 基因表示。HNF4 的 Overexpression 增加了 ACAT2 表示,而 HNF4 击倒减少的 ACAT2 表示。Peroxisome 激活 proliferator 的受体 gamma 激活剂 1 (PCG1 ) , HNF4 的激活剂,,增加了 ACAT2 表示小 heterodimer 搭挡(SHP ) , HNF4 的 corepressor,减少的 ACAT2 表示。这些结果提供更多的卓见进 ACAT2 表示的 transcriptional 规定。 | Zhuqin Zhang Jinjing Liu Yang Xi Ruifeng Yang Houzao Chen Zhenya Li Depei Liu Chihchuan Liang | 2012 | Acta Biochimica et Biophysica Sinica2012,44,2: | 1 |
| 8 | Use of a high thoracic epidural analgesia for treatment of end-stage congestive heart failure secondary to coronary artery disease显示文摘 | Wu Shuang Fu Shiying Liu Fengqi Qu Renhai Wang Lanfeng Li Zhuqin Wang Xu | 2007 | International Journal of Cardiology2007,,2: | 1 |
| 9 | Extreme learning machine:theory and applications显示文摘 | Bin Huangguang Yu Zhuqin | | 0,,: | 1 |
| 10 | What to Follow "Make" and What to Follow "Do"——Corpus-based Study on the De-lexical Use of "make" and "do" in Native Speakers' and Chinese Students' Writing显示文摘 | Zhuqin Fu | 2006 | 美中教育评论2006,3,5: | 1 |
| 11 | The Role of Communicative Drills in Communicative Language Teaching显示文摘 | Zhuqin Fu | 2005 | Sino-US English Teaching2005,2,5: | 0 |
| 12 | Systems biomedicine: It's your turn --Recent progress in systems biomedicine显示文摘 | Zhuqin Zhang Zhiguo Zhao Bing Liu Dongguo Li Dandan Zhang Houzao Chen Depei Liu | 2013 | Frontiers of Electrical and Electronic Engineering in China2013,8,2: | 0 |
| 13 | Effect of Different Pollination Varieties on Qingxiang Pear Fruit Quality显示文摘With Qingxiang pear as test material,we study the effect of different pollination varieties on Qingxiang pear fruit quality. The results show that Xinshiji,Xizilu,Cuiguan and Yuanhuang as the pollination varieties for Qingxiang pear can create the best comprehensive quality,and these varieties can be chosen in production as the pollination varieties for Qingxiang pear,followed by Cuilu and Xishui. | Zhuqin LIU Jinhui CHEN Yunting ZHENG Guoqiang JIANG | 2016 | Asian Agricultural Research2016,8,11: | 0 |