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| 1 | 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 |
| 2 | Overexpression of a dominant-negative mutant of SIRT1 in mouse heart causes cardiomyocyte apoptosis and early-onset heart failure显示文摘SIRT1,a mammalian ortholog of yeast silent information regulator 2(Sir2),is an NAD+-dependent protein deacetylase that plays a critical role in the regulation of vascular function.The current study aims to investigate the functional significance of deacetylase activity of SIRT1 in heart.Here we show that the early postnatal hearts expressed the highest level of SIRT1deacetylase activity compared to adult and aged hearts.We generated transgenic mice with cardiac-specific expression of a dominant-negative form of the human SIRT1(SIRT1H363Y),which represses endogenous SIRT1 activity.The transgenic mice displayed dilated atrial and ventricular chambers,and died early in the postnatal period.Pathological,echocardiographic and molecular phenotype confirmed the presence of dilated cardiomyopathy.Terminal deoxynucleotidyl transferase-mediated dUTP nick-end-labeling analysis revealed a greater abundance of apoptotic nuclei in the hearts of transgenic mice.Furthermore,we show that cardiomyocyte apoptosis caused by suppression of SIRT1 activity is,at least in part,due to increased p53acetylation and upregulated Bax expression.These results indicate that dominant negative form of SIRT1(SIRT1H363Y)overexpression in mouse hearts causes cardiomyocyte apoptosis and early-onset heart failure,suggesting a critical role of SIRT1 in preserving normal cardiac development during the early postnatal period. | MU WenLi ZHANG QingJun TANG XiaoQiang FU WenYan ZHENG Wei LU YunBiao LI HongLiang WEI YuSheng LI Li SHE ZhiGang CHEN HouZao LIU DePei | 2014 | Science China(Life Sciences)2014，57，9： | 12 |
| 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 | Baicalein protects against the development of angiotensin II-induced abdominal aortic aneurysms by blocking JNK and p38 MAPK signaling显示文摘An abdominal aortic aneurysm(AAA) is a permanent, localized dilatation of the abdominal aorta. In western countries, the morbidity of AAA is approximately 8%. Currently, pharmacotherapies for AAA are limited. Here, we demonstrate that baicalein(BAI), the main component of the Chinese traditional drug 'Huang Qin', attenuates the incidence and severity of AAA in Apoe儃/儃 mice infused with angiotensin II(AngII). Mechanically, BAI treatment decreases AngII-induced reactive oxygen species(ROS) production in the aortic wall. Moreover, BAI inhibits inflammatory cell accumulation in the aortas of mice infused with AngII. It also inhibits AngII-induced activation of matrix metalloproteinase 2(MMP-2) and MMP-9 to maintain elastin content in vivo. In addition, it blocks AngII cascade by downregulating angiotensin type 1 receptor(AT1R) and inhibiting mitogen-activated protein kinases(MAPKs). Taken together, our findings show that BAI is an effective agent for AAA prevention. | Fang Wang Houzao Chen Yunfei Yan Yue Liu Shuyang Zhang Depei Liu | 2016 | Science China(Life Sciences)2016，59，9： | 7 |
| 5 | 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 |
| 6 | SIRT1 inhibits angiotensin Ⅱ-induced vascular smooth muscle cell hypertrophy显示文摘血管收缩素 II (Ang II ) 刺激脉管的光滑的肌肉房间(VSMC ) 肥大作为在象动脉粥样硬化那样的脉管的疾病的发展的一个批评事件。Sirtuin (SIRT ) 1,菸碱腺嘌 dinucleotide 依赖者 deacetylase,被表明了由支持脉管的松驰和减少的巨噬细胞泡沫房间形成,而是它在 VSMC 肥大的角色仍然是的内皮细胞层依赖者在动脉粥样硬化施加保护的效果未知。在这研究,我们试着在 Ang 导致 II 的 VSMC 肥大上调查 SIRT1 的效果。结果显著地显示出 SIRT1 的那调停 adenoviral 的在表示上禁止的 Ang 导致 II 的 VSMC 肥大,当时由 RNAi 的 SIRT1 击倒导致了一增加[3H ] VSMC 的白氨酸加入。因此,菸碱腺嘌 dinucleotide 磷酸盐 oxidase 1 (Nox1 ) Ang II 导致的表示被 SIRT1 在 VSMC 禁止。SIRT1 使活跃之物 resveratrol 减少了,而内长的 SIRT1 禁止者菸碱在 A7r5 VSMC 增加了 Nox1 表示。而且,抄写因素 GATA-6 被 SIRT1 涉及 Nox1 表示的下面规定。这些结果由压制 Ang 提供新卓见进 SIRT1 的 anti-atherogenic 性质导致 II 的 VSMC 肥大。 | Li Li Peng Gao Huina Zhang Houzao Chen Wei Zheng Xiang Lv Tingting Xu Yusheng Wei Depei Liu Chihchuan Liang | 2011 | Acta Biochimica et Biophysica Sinica2011，43，2： | 6 |
| 7 | 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 |
| 8 | A vascular endothelial growth factor activating transcription factor increases the endothelial progenitor cells population and induces therapeutic angiogenesis in a type 1 diabetic mouse with hindlimb ischemia显示文摘 | Diao Yongpeng Lian Lishan Guo Lilong Chen Houzao Chen Yuexin Song Xiaojun Li Yongjun | 2014 | Chinese Medical Journal2014，，20： | 3 |
| 9 | 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 |
| 10 | Endothelium-specific overexpression of class Ⅲ deacetylase SIRT1 decreases atherosclerosis in apolipoprotein E-deficient mice显示文摘 | Zhang Qinjun Wang Zhao Chen Houzao | 2008 | Cardiovasc Res2008，80，2： | 1 |
| 11 | SIRT1 suppresses activator protein-1 transcriptional activity and cyclooxygenase-2 expression in maerophages显示文摘 | ZHANG Ran CHEN Houzao LIU Jinjing | 2010 | J Biol Chem2010，285，： | 1 |
| 12 | Oxidative stress in atrial fibrillation: An emerging role of NADPH oxidase显示文摘 | Ji-Youn Youn Jun Zhang Yixuan Zhang Houzao Chen Depei Liu Peipei Ping James N. Weiss Hua Cai | 2013 | Journal of Molecular and Cellular Cardiology2013，，： | 1 |
| 13 | Mechanistic perspectives of calorie restriction on vascular homeostasis显示文摘Calorie restriction(CR)is a dietary regime based on low calorie intake.CR without malnutrition extends lifespan in a wide range of organisms from yeast to rodents,and CR can prevent and delay the onset of age-related functional decline and diseases in human and non-human primates.CR is a safe and effective intervention to reduce vascular risk factors in humans.In recent years,studies in rodents have provided mechanistic insights into the beneficial effects of CR on vascular homeostasis,including reduced oxidative stress,enhanced nitric oxide(NO)bioactivity,and decreased inflammation.A number of important molecules,including sirtuins,AMP-activated protein kinase,mammalian targets of rapamycin,endothelial nitric oxidase and their regulatory pathways are involved in the maintenance of vascular homeostasis.Evidence has shown that these pathways are responsible for many aspects of CR’s effects,and that they may also mediate the effects of CR on vasculature. | LIU Yue CHEN HouZao LIU DePei | 2014 | Science China(Life Sciences)2014，57，8： | 0 |
| 14 | 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 |
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