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作者： nanping wang institute of cardiovascular science and diabetes center,peking university,beijing 100191

Emerging evidence has revealed potential implications of peroxisome proliferator-activated receptor-δ(PPAR-δ) in lipid homeostasis,insulin resistance and cardiovascular ***,its pathophysiological roles and the underlying mechanisms remain to be *** functional genomic approach including gain- and loss-of-function studies,we have examined the effects of PPAR-8 on the expression of genes involved in the lipid biosynthesis in hepatocytes and the in vascular endothelial activation,major pathophysiological processes associated with metabolic *** results have demonstrated that,in hepatocytes,PPAR-δagonist as well as overexpression of PPAR-δinduced the gene expression of Insig-1,a regulatory endoplasmic reticulum protein braking SREBP activation. PPAR-δinhibited the proteolytic processing of the SREBP-1 into the mature active form,thereby suppressing the expression of the lipogenic genes such as fatty acid synthase,stearyl CoA desaturase-I and glycerol-3-phosphate *** effect is achieved by the induction of Insig-1,a direct target gene for PPAR-δFurthermore,overexpression of PPAR-δinduced Insig-1 expression and suppressed SREBP-1 activation,hence,limiting hepatic steatosis in obese diabetic *** vascular endothelial ceils (ECs),PPAR-δligands significantly inhibited TNF-α-induced expression of vascular cell adhesion molecule-1 and E-selectin as well as the ensuing endothelial-leukocyte ***-δligand upregulated the expression of antioxidant genes and decreased reactive oxygen species production in ECs. Ligand activation switched the association of BCL-6,a transcription repressor,from PPAR-δto the vascular cell adhesion molecule (VCAM)-1 *** interfering RNA reduced endogenous PPAR-δexpression but potentiated the suppressive effect of GW0742 on EC activation,suggesting that the nonliganded PPAR-δmay have an opposite *** together,our study reveals novel functions and the mechanism by which PPAR-δr

关键词： Nuclear receptor transcription factor lipogenesis gene expression diabetes

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Role of inositol 1,4,5-trisphosphate receptors in α1-adrenergic receptorinduced cardiomyocyte hypertrophy

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Acta Pharmacologica Sinica 2006年第7期27卷 895-900页

作者： Da-li LUO~(2,3,5) Jian GAO~2 Xiao-mei LAN~3 Gang wang~4 Sheng WEI~4 Rui-ping XIAO~4 Qi-de HAN~32 Department of Pharmacology,School of Chemical Biology & Pharmaceutical sciences,Capital university of Medical sciences,beijing 100069,China 3 institute of cardiovascular science at Health science center,peking university beijing 100083,China 4 institute of Molecular Medicine and College of Life science,peking university,beijing 100871,China Department of Pharmacology School of Chemical Biology & Pharmaceutical Sciences Capital University of Medical Sciences Beijing China institute of cardiovascular science at Health science center Peking University Beijing China institute of Molecular Medicine and College of Life science Peking University Beijing China

Aim:Intracellular Ca2+plays pivotal roles in diverse cellular functions,includinggene transcription that underlies cardiac remodeling during stress ***,the role of inositol 1,4,5-trisphosphate receptors（IP3Rs）in the media-tion of cardiac intracellular Ca2+and hypertrophic growth remains *** with neonatal rat ventricular myocytes suggests that activation of IP3Rsmay be linked to α1adrenergic receptor（α1AR）increased stereotyped Ca2+sparkoccurrence and global Ca2+***,we hypothesized that Ca2+releasethrough IP3Rs was necessary for α1AR-stimulated cardiac ***:We used myoinositol 1,4,5-trisphosphate hexakis（butyryloxymethyl）ester（IP3BM）,a membrane-permeant ester of IP3,to activate IP3Rs directly,and Fluo 4/AM tomeasure intracellular Ca2+***:IP3BM(10μmol·L-1)mimicked theeffects of phenylephrine,a selective agonist of α1AR,in increments in local Ca2+spark release（especially in the perinuclear area）and global Ca2+*** importantly,IP3R inhibitors,2-aminoethoxydiphenyl borateand Xestospongin C,abolished the IP3BM-induced Ca2+responses,and signifi-cantly suppressed α1AR-induced cardiomyocyte hypertrophy assayed by cellsize,[3H]leucine incorporation and atrial natriuretic factor gene expression,dur-ing sustained（48 h）phenylephrine ***:These results,therefore,provide cellular mechanisms that link IP3R signaling to α1AR-stimulatedgene expression and cardiomyocyte hypertrophy.

关键词： inositol 1,4,5-trisphosphate receptors Ca2+sparks α1 adrenergic stimulation cardiac hypertrophy

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Internalization and distribution of three α1-adrenoceptor subtypes in HEK293A cells before and after agonist stimulation

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Acta Pharmacologica Sinica 2007年第3期28卷 359-366页

作者： Shu-yi wang~2 Yao SONG~2 Ming XU~2 Qi-hua HE~3 Qi-de HAN~2 You-yi ZHANG~(2,4)2 institute of Vascular Medicine,peking university Third Hospital and Key Laboratory of Molecular cardiovascular sciences,Ministry of Education,beijing 100083,China 2 center of Medical Analysis,peking university,Health science center,beijing 100083,China institute of Vascular Medicine Peking University Third Hospital and Key Laboratory of Molecular Cardiovascular Sciences Ministry of Education Beijing China center of Medical Analysis Peking University Health Science Center Beijing China

Aim:To examine the subcellular distribution of the 3 α1-adrenoceptor（α1-AR）subtypes and their internalization and trafficking upon agonist stimulation in hu-man embryonic kidney 293A ***:Confocal real-time imaging,enzymelinked immunosorbent assay（ELISA）and whole cell[3H]-prazosin binding assaywere applied to detect the distribution and localization of the 3 α1B-AR ***:α1A-AR was found both on the cell surface and in the cytoplasm;α1B-AR,however,was predominantly detected on the cell surface,while α1D-AR wasdetected mainly in the intracellular *** stimulation withphenylephrine,localization changes were detected by confocal microscopy forα1A-and α1B-AR, but the localization of α1D-AR were *** promoted a more rapid internalization of α1B-AR than α1A-AR.α1D-ARinternalization was detected only by *** cell[3H]-prazosin bindingassay showed that α1A-AR functional receptors were detected both on the cellsurface and in the cytoplasm;α1B-AR,however,were detected predominantly onthe cell surface,while α1D-AR were detected mainly in intracellular *** stimulation promoted internalization of α1A-and α***:Phenylephrine stimulation induced changes in the localization of the3α1-AR.

关键词： adrenoceptor agonist stimulation confocal image enzyme-linked immunosorbent assay [~3H]-prazosin binding assay internalization subcellular distribution subtype

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Taurine antagonized oxidative stress injury induced by homocysteine in rat vascular smooth muscle cells

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Acta Pharmacologica Sinica 2004年第3期25卷 87-92页

作者： Lin CHANG2,3,Jian-xin XU4,Jing ZHAO5,Yong-zheng PANG2,3,Chao-shu TANG2,3,Yong-fen QI5,6 2institute of cardiovascular Diseases,the FirstHospital,peking university,beijing 100034 3institute of cardiovascular Diseases,peking university,beijing 100083 4instituteof Biophysics,Chinese Academy of sciences,beijing 100101 5Department of Physiology,Health science center,peking university,beijing 100083,China institute of cardiovascular Diseases the First Hospital Peking University 北京 100034 institute of Biophysics Chinese Academy of Sciences 北京 100101 Department of Physiology Health Science Center Peking University 北京 100083

AIM: To observe protective effects of taurine on reactive oxygen species generation induced by homocysteine in rat vascular smooth muscle cells (VSMC). METHODS: Rat VSMC was incubated with various concentrations of homocysteine and taurine. The lactate dehydrogenase (LDH) activity which released into culture medium was elevated as an indicator for VSMC injury. The reactive oxygen species (ROS) — hydrogen peroxide (H2O2) and superoxide anion (O2ˉ· )were measured with luminol or lucigenin chemiluminescences method, and the mitochondria Mn-superoxide dismutase (Mn-SOD) and catalase (CAT) were also measured in treated VSMC. RESULTS: LDH leakage from cultured VSMC treated with homocystenie, was increased (P0.05 vs control). In this study, the superoxide anion in VSMC was not detectable by chemiluminent method. In addition, treatment of VSMC with taurine increased mitochondria Mn-SOD and CAT activity in a concentration dependent manner (P<0.05), but homocysteine decreased mitochondria Mn-SOD and CAT activity (P<0.01 vs control). In addition, co-administration of taurine markedly ameliorated homocysteine-induced inhibition of Mn-SOD and CAT activity in VSMC (P<0.01 vs homocysteine alone group). CONCLUSION: Taurine antagonized the effects of homocysteine on ROS generation and anti-oxidant enzyme activities in rat VSMC in vitro.

关键词： homocysteine taurine vascular smooth muscle mitochondria reactive oxygen species

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Taurine inhibits ischemia/reperfusion-induced compartment syndrome in rabbits

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Acta Pharmacologica Sinica 2005年第7期26卷 821-827页

作者： Ji-xian wang~(2,3) Yan LI~2 Li-ke ZHANG~4 Jing ZHAO~5 Yong-zheng PANG~(2,3) Chao-shu TANG~(3,5) Jing ZHANG~(2,3,6) 1 institute of cardiovascular Disease Research,The First Hospital of peking university,beijing 100034,China 3 Key Laboratory of Molecular cardiovascular science,Ministry of Education,beijing 100083,China 4 Department of Pathophysiology,Capital institute of Medicine,beijing 100054,China 5 Department of Physiology Health center of Medical sciences,peking university,beijing 100083,China institute of cardiovascular Disease Research The First Hospital of Peking University Beijing China Key Laboratory of Molecular cardiovascular science Ministry of Education Beijing China Department of Pathophysiology Capital Institute of Medicine Beijing China Department of Physiology Health Center of Medical Sciences Peking University Beijing China

Aim:To investigate effects of taurine on ischemia/reperfusion(I/R)-induced com-partment syndrome in rabbit hind ***:Rabbits underwent femoralartery occlusion after ligation of branches from terminal aorta to femoral *** a 7-h ischemia,reperfusion was established with the use of heparinizedpolyethylene *** received taurine(1 g/kg)or normal saline(control)by iv infusion 10 min before shunt *** reperfusion,anterior com-partment pressure(ACP)was monitored continuously in the left lower *** muscle triphenyltetrazolium chloride(TTC)level,taurine contentand myeloperoxidase activity were *** stress was induced in thein vitro gastrocnemius muscle slices by free radical generating systems(FRGS),and the malondialdehyde content was measured in presence or absence of ***:After 7 h of ischemia,none of the parameters that we measured weredifferent from those before ischemia,except that TTC reduction decreased by80%.In the control group,after 2 h of reperfusion,ACP increased 4.5-fold,andgastrocnemius muscle taurine content was reduced by 33%.In taurine-treatedanimals,at 2 h reperfusion,the mean arterial blood pressure and heart rate wereincreased,by 6% and 10%.ACP decreased by 39%,muscle edema decreased by16%,TTC reduction increased by 150%,and lactate dehydrogenase decreased by36% compared to control *** and muscle taurine content increased by70% and 88%,*** the taurine-treated group,at 2 h repeffusion,plasmamalondialdehyde and conjugated diene content were decreased by 38% and 23%,respectively,and muscle malondialdehyde and conjugated diene content decreasedby 22% and 30%,respectively compared to the control *** 2 h reperfusion,myeloperoxidase activity was increased 3.5-fold in control *** the in vitrostudy,taurine decreased malondialdehyde content in muscle slices incubatedwith hypochlorous acid in a dose-dependent manner,but there was no changewhen incubated

关键词： taurine compartment syndromes reperfu sion injury

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Clinical application and management of temporary mechanical circulatory support:A clinical consensus

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Chinese Medical Journal 2024年第10期137卷 1135-1139页

作者： Nianguo Dong Liangwan Chen Xin Chen Huishan wang Yingbin Xiao Xianqiang wang Jinsong Huang Yang Yan Pramod Bonde Neel Sodha Pavan Atluri Juan Pablo Maureira AndréVincentelli Masanobu Yanase Yixuan wang Haitao Zhang Xiaotong Hou Yoshijuki Takami Pascal Leprince Thierry Folliguet Frank W Sellke Chinese Society for Thoracic and cardiovascular Surgery Chinese Association of cardiovascular Surgeons Cardiac Critical Care Professional Committee of Chinese Medical Association Chinese Society of Extracorporeal Life Support European Society of cardiovascular and Endovascular Surgery French Society of Thoracic and cardiovascular Surgery Japanese Society for cardiovascular Surgery Japanese Society of Artificial Organs Department of cardiovascular Surgery Union Hospital of Tongji Medical CollegeHuazhong University of Science and TechnologyWuhanHubei 430022China Department of cardiovascular Surgery Fujian Medical University Union HospitalFuzhouFujian 350000China Department of Thoracic and cardiovascular Surgery Nanjing First HospitalNanjing Medical UniversityNanjingJiangsu 210000China Department of cardiovascular Surgery General Hospital of Northern Theater CommandShenyangLiaoning 110000China Department of cardiovascular Surgery Xinqiao HospitalThird Military Medical UniversityChongqing 400037 China Department of cardiovascular Surgery Fuwai HospitalNational Center for Cardiovascular DiseasesChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100000 China Department of cardiovascular Surgery Guangdong Provincial Cardiovascular InstituteGuangdong General HospitalGuangdong Academy of Medical SciencesGuangzhouGuangdong 510000 China Department of cardiovascular Surgery First Affiliated Hospital of Xi’an Jiaotong UniversityXi’anShaanxi 710061China Department of Cardiac Surgery Yale School of Medicine330 Cedar St204 BoardmanNew HavenCT 06510USA Department of Cardiothoracic Surgery Alpert Medical SchoolBrown University Rhode Island HospitalProvidenceRI 02912USA Department of cardiovascular Surgery Department of SurgeryUniversity of PennsylvaniaPhiladelphiaPA 19113USA Department of cardiovascular Surgery and Transplantation University Hospital of NancyUniversity of LorraineVandoeuvre-lès-Nancy 54500France Department of cardiovascular Surgery University Hospital of LilleUniversity of LilleLille 59037France Department of Cardiology Fujita Health University School of MedicineToyoakeAichi 470-1192Japan Department of Adult Surgical Intensive Care Unit Fuwai HospitalNational Center for Cardiovascular DiseasesChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100000China Department of Cardiac Intensive Care Beijing Institute of HeartLung and B

Temporary mechanical circulatory support(tMCS)plays a pivotal role in managing severe or refractory cardiogenic shock(CS),furnishing essential hemodynamic support,and sustaining organ perfusion from hours to weeks,or to even *** the past decade,the utilization of tMCS has witnessed a signicant increase in American and European *** in Asia,the newly developed concepts and devices constituting tMCS have also made rapid ***,the absence of a consensus or standardized guidelines,especially for the Asian population considering inherited polymorphism,is *** address this knowledge gap,eight associations/societies and experts in thiseld came up with the present consensus after repeated discussions,more specically for the Asian *** comprehensively elucidates the commonly employed tMCS devices,criteria for patient selection,indications and contraindications,clinical management,and the optimal timing for implantation and *** goal of this statement is to promote the standardized application of tMCS and make reasonable decisions in clinical ***-length version of the consensus can be seen in Supplementary File,http://***/CM9/B883.

关键词： application statement discussions

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Hydrogen sulfide ameliorates vascular calcification induced by vitamin D3 plus nicotine in rats

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Acta Pharmacologica Sinica 2006年第3期27卷 299-306页

作者： Sheng-ying WU~(2,6) Chun-shui PAN~3 Bin GENG~3 Jing ZHAO~3 Fang YU~3 Yong-zheng PANG~3 Chao-shu TANG~4 Yong-fen QI~(3,4,5) ~2institute of cardiovascular Disease,peking university First Hospital.beijing 100034 ~3Department of Physiology and Pathophysiology,peking university Health science center,beijing 100083,China,~4Key Laboratory of Molecular cardiovascular science,Ministry of Education,beijing 100083,China institute of cardiovascular Disease Peking University First Hospital Beijing China Department of Physiology and Pathophysiology Peking University Health Science Center Beijing China Key Laboratory of Molecular cardiovascular science Ministry of Education Beijing China

Aim:To investigate the role of the endogenous cystathionine γ-synthase(CSE)/hydrogen sulfide(H2S)pathway in vascular calcification in ***:A ratvascular calcification model was established by administration of vitamin D3 plusnicotine(VDN).The amount of CSE and osteopontin(OPN)mRNA was deter-mined by using semi-quantitative reverse-transcription polymerase chain *** calcium content,45Ca2+accumulation and alkaline phosphatase(ALP)activitywere measured.H,S production and CSE activity were ***:yonKossa staining produced strong positive black/brown staining in areas amongthe elastic fibers of the medial layer in the calcified *** calcium content,45Ca2+accumulation and ALP activity in calcified arteries increased by 6.77-,1.42-,and 1.87-fold,respectively,compared with *** expression of the OPNgene was upregulated(P<0.01).Expression of the CSE gene was ***,calcium content,45Ca2+uptake and ALP activity in the VDN plus NaHSgroup was lower than that in the VDN *** content of calcium and45Ca2+accumulation and activity of ALP in the aorta were 34.8%,40.75% and 63.5% lowerin the low-dosage NariS group than in the VDN group,respectively(P<0.01),andthe calcium content and deposition of45Ca2+and activity of ALP was 83.9%,37.8 % and 46.2% lower in the aorta in the high-dosage NariS group than in theVDN group,respectively(P<0.01).The expression of the OPN gene ***:The production of H,S,and CSE activity were de-creased and CSE gene expression was downregulated in rats with vascularcalcification.H2S can ameliorate vascular calcification,suggesting that the H2S/CSE pathway plays a regulatory role in the pathogenesis of vascular calcification.

关键词： hydrogen sulfide cystathionine-lyase vascular calcification mRNA

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Real-time detection of α1A-AR movement stimulated by phenylephrine in single living cells

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Acta Pharmacologica Sinica 2007年第6期28卷 796-802页

作者： Ning XU~(2,5),Zhang-yi LIANG~(3,5),Ming XU~2,Ying-hua GUAN~3,Qi-hua HE~4,Qi-de HAN~2,Xin-sheng ZHAO~(3,6),You-yi ZHANG~(2,6)~2 institute of Vascular Medicine,peking university Third Hospital,and Key Laboratory of Molecular cardiovascular sciences,Ministry ofEducation,beijing 100083,China ~3 beijing National Laboratory for Molecular sciences,State Key Laboratory for Structural Chemistry ofUnstable and Stable Species,and Department of Chemical Biology,College of Chemistry and Molecular Engineering,peking university,beijing 100871,China ~4 center of Medical Analysis,peking university,Health science center,beijing 100083,China institute of Vascular Medicine Peking University Third Hospital and Key Laboratory of Molecular Cardiovascular Sciences Ministry of Education Beijing China beijing National Laboratory for Molecular sciences State Key Laboratory for Structural Chemistry of Unstable and Stable Species Department of Chemical Biology College of Chemistry and Molecular Engineering Peking University Beijing China center of Medical Analysis Peking University Health Science Center Beijing China

Aim:To investigate the movement of α1A-adrenergic receptors(α1A-AR) stimu-lated by agonist,phenylephrine （PE）,and the dynamics of receptor movement inreal time in single living cells with millisecond ***:We labeledα1A-AR using the monoclonal,anti-FLAG （a kind of tag） antibody and Cy3-conju-gated goat anti-mouse IgG and recorded the trajectory of their transport processin living HEK293A cells stimulated by agonist,PE,and then analyzed their dy-namic ***:The specific detection of α1A-AR on the surface ofliving HEK293A-α1Acells was achieved.α1A-AR internalize under the stimulationof *** the cells were stimulated with PE for 20 min,apparent colocalizationwas found between α1A-AR and *** 40 min stimulation of PE,trajecto-ries of approximate linear motion in HEK293A-α1Acells were recorded,and theirvelocity was ***:The specific labeling method on the livingcell surface provides a convenient means of real-time detection of the behavior ofsurface *** this method we were able to specifically detect α1A-AR andrecord the behavior of individual particles of receptors with 50 ms exposure time inreal time in single living cells.

关键词： adrenergic receptor trajectory living cell

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Age-associated alternations in cardiac β-adrenergic receptor signaling

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Journal of Geriatric Cardiology 2005年第4期2卷 254-257页

作者： Jing MA, Shiwen wang, Ruiping XIAO The institute of Molecular Medicine & the institute of cardiovascular science, peking university, beijing 100871, China The institute of Geriatric Cardiology, Chinese PLA General Hospital, beijing 100853, China Laboratory of cardiovascular science, Gerontology Research center, National institute on Aging, Baltimore, MD 21224, USA The institute of Molecular Medicine & the institute of cardiovascular science Peking University Beijing 100871 China The institute of Geriatric Cardiology Chinese PLA General Hospital Beijing 100853 China Laboratory of cardiovascular science Gerontology Research Center National Institute on Aging Baltimore MD 21224 USA

During aging, cardiac contractile response to β-AR stimulation is decreased in humans and animal models. Recent studies demonstrate that the positive inotropic effects of both β1-AR and β2-AR stimulation are significantly decreased with *** is accompanied by decreases in both β-AR subtype densities and a reduction in membrane adenylyl cyclase activity. However,neither G protein-coupled receptor kinases (GRKs) nor inhibitory G proteins (Gi) appears to contribute to the age-associated reduction in the β-AR modulation of contraction. Thus, while both aging and chronic heart failure exhibit a diminution in cardiac β-AR responsiveness, only heart failure exhibits increased GRK-mediated desensitization ofβ-Ars and an upregulation of Gi proteins.

关键词： Nature adrenergic receptor signaling Age-associated alternations in cardiac

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Receptor subtype involved in α-adrenergic receptor-mediated Ca2+ signaling in cardiomyocytes

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Acta Pharmacologica Sinica 2007年第7期 968-974页

作者： Da-li LUO~(2,3,4),Jian GAO~2,Lin-lin FAN~2,Yu TANG~2,You-yi ZHANG~3,Qi-de HAN~3~2 Department of Pharmacology,School of Chemical Biology and Pharmaceutical sciences,Capital university of Medical sciences,beijing100069,China ~3 institute of cardiovascular science at the Health science center,peking university,beijing 100083,China

Aim:The enhancement of intracellular Ca2+signaling in response to α1-adrener-gic receptor （α1-AR） stimulation is an essential signal transduction event in theregulation of cardiac functions,such as cardiac growth,cardiac contraction,andcardiac adaptation to various *** present study was intended todetermine the role（s） of the α1-AR subtype（s） in mediating this ***:We evaluated the effects of subtype-specific agonists and antagonists of the α1-AR on the intracellular Ca2+signaling of neonatal rat ventricular myocytes usinga confocal ***:After being cultured for 48 h,the myocytesexhibited spontaneous local Ca2+release,sparks,and global Ca2+*** of the α1-AR with phenylephrine,a selective agonist of the α1-AR,dose-dependently increased the frequency of Ca2+transients with an EC50valueof 2.3 μmol/*** the α1A-AR subtype with 5-methylurapidil （5-Mu） inhi-bited the stimulatory effect of phenylephrine with an IC50value of 6.7 nmol/***,blockade of the α1B-AR and α1D-AR subtypes with chloroethylclonidineand BMY 7378,respectively,did not affect the phenylephrine ***,thelocal Ca2+spark numbers were also increased by the activation of the α1-AR,andthis effect could be abolished selectively by *** importantly,A61603,anovel selective α1A-AR agonist,mimicked the effects of phenylephrine,but withmore potency (EC50value=6.9 nmol/L) in the potentiation of Ca2+transients,andblockade of the α1A-AR by 5-Mu caused abolishment of its ***:These results indicate that α1-adrenergic stimulation of intracellular Ca2+activityis mediated selectively by the α1A-AR.

关键词： α1-adrenergic receptor subtype cardiomyocyte Ca2+ signaling A61603

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