张寄南
蛋白质磷酸化、心肌病分子蛋白质发病基础、心脏标志物应用等方面
个性化签名
- 姓名:张寄南
- 目前身份:
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学术头衔:
博士生导师
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学科领域:
内科学
- 研究兴趣:蛋白质磷酸化、心肌病分子蛋白质发病基础、心脏标志物应用等方面
张寄南教授是南京医科大学第一附属医院心脏科主任医师、博士生导师、享受国务院特殊津贴,是江苏省135重点实验室”临床生物学诊断与治疗实验室”学科带头人。担任中国病理生理受体学术委员会副主任委员、中国临床受体委员会副主任委员、连续三届江苏省自然科学基金委员会委员、江苏省生物医学工程学会基因蛋白质分会副主任委员,曾获得2001年度全国优秀科技工作者称号。张寄南教授从事医学研究、教学、临床工作45年,在蛋白质磷酸化、心肌病分子蛋白质发病基础、心脏标志物应用等方面做了重要工作。主持和参与省重点重大项目、国家级及国家攻关项目累计 22项。自1997年以来共获省部级奖项9次,获专利3项,新药证书1项。发表论文130余篇,其中SCI收录25篇,主编学术专著2部,对国内心血管病基础与临床结合、自主创新研究有积极影响。
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【期刊论文】A Novel Protein Interacts with the Major Transforming Growth Factor-
张寄南, Manfred A Sandler, Ji-Nan Zhang, Donald R. Westerhausen, Jr., andJ oseph J. Billadello
The Journal of Biological Chemistry Vol. 269, No. 34, Issue of August 26, pp. 21500-21504, 1994,-0001,():
-1年11月30日
Multiple transforming growth factor-ß (TGF-ß) responsive elements have been identified within the 5’-flanking region of the plasminogen activator inhibitor type-1 (PAI-1) gene. This study was designed to characterize the major TGF-ß responsive element (-804 to -546). DNA footprint assays showed that the region of protein contact (-726 to -703) did not include consensus sequences for any known transacting factors. The results of UV cross-linking and Southwestern blot experiments showed that a protein of M, 100,OOO specifically binds to the TGH-ß responsive element and that this protein undergoes post-transcriptional activation within 5 min after stimulation of Hep G2 cells by TGF-ß resulting in a marked increase in affinity for the target DNA sequence. These results show that stimulation of Hep G2 cells with TGF-ß increases the affinity of a novel pr 100-kDa protein for the major TGF-ß responsive element within the PAI-1 gene.
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张寄南, ZHANG Ji-Nan, GENG Qian, CHEN Xiang-Jian, FANG Wu-Wang, WU Xiao-Hui, YANG Di
Zhang JN et al. Acta Pharmacol Sin 2003, Nov; 24 (11): 1099-1102,-0001,():
-1年11月30日
AIM: To investigate the changes of cardiac calcium handling proteins and endothelin system in dilated cardiomyopathy (DCM) rats and the effects of perindopril and bisoprolol on the remodeling ventricles. METHODS: DCM rats were employed using a 2-kidney, 1-clip hypertensive and diabetic model. Some of the DCM rats were treated with perindopril and bisoprolol for 3 months, respectively. The ratio of left ventricular weight to body weight (LVW/BW), mRNA expressions of calcium handling proteins and endothelin receptors were determined. The alterations of maximum binding capacity (Bmax) and equilibrium dissociation constant (KD) values of cardiac endothelin receptors (ETR) and its subtypes were detected. RESULTS: Compared with those of normal control, blood pressure, and LVW/BW in the DCM rats were elevated. Sarcoplasmic reticulum calcium pump (SERCA) mRNA expression and SERCA activity decreased in the left ventricle. The ETR Bmax decreased, especially the endothelin receptor A. Endothelin converting enzyme activity and expression were elevated, and mRNA expressions of β1-adrenoreceptor and inositol-3-phosphate receptor in some hearts increased as well. The administration of perindopril and bisoprolol could reverse myocardial hypertrophy and restore the imbalance of calcium handling proteins and endothelin system. CONCLUSION: The disorder of calcium handling proteins and endothelin system existed in the hearts of DCM rats. Treatment of perindopril and bisoprolol could reverse myocardial hypertrophy and changes in DCM rats.
congestive cardiomyopathy, ventricular remodeling, adrenergic receptors, calcium, endothelin receptors
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张寄南
中华心血管病杂志1999年12月第27卷第6期/Chin J Cardiol, December 1999, Vol. 27, No. 6,-0001,():
-1年11月30日
目的 全国十二家大型医院协作观察中西医结合治疗急性病毒性心肌炎疗效。方法 对1 028 例临床诊断为急性病毒性心肌炎患者随机各分两组,治疗组602 例,用中西医结合(黄芪、牛磺酸、泛葵利酮、抗心律失常药等) 治疗;对照组426 例,用常规(极化液、抗心律失常药等) 治疗。结果 中西医结合治疗组临床症状改善、外周血肠道病毒阴转、心电图ST2T改变及房室传导阻滞、阵发性心房颤动、窦房传导阻滞等恢复均优于对照组( P < 0. 01、0. 05) ;对早搏及心功能改善两组间无统计学差异( P < 0. 05) 。结论 在目前对急性病毒性心肌炎无特效药物治疗的情况下,采用中西医结合治疗可作为一种治疗手段。
心肌炎, 心律失常, 干预性研究
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张寄南, Di Yang, , Pascale Gluais, Ji Nan Zhang, Paul M. Vanhoutte, Michel Fe
Blackwell Publishing Fundamental & Clinical Pharmacology 18 (2004) 321-326,-0001,():
-1年11月30日
The present study was designed to determine whether or not an increase in endothelial intracellular concentration of calcium ([Ca2+]i) evokes endotheliumdependent contractions in the aorta from normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). Acetylcholine, adenosine triphosphate (ATP) and the calcium ionophore, A 23187, produced endothelium-dependent relaxations in isolated aortic rings of both WKY and SHR. These relaxations in response to the three agonists were significantly smaller in the SHR when compared with the WKY. Endothelium-dependent contractions to acetylcholine, ATP and A 23187 were observed only in the aorta isolated from the SHR. In the presence of NG-nitro-Larginine, an NO synthase inhibitor, the endothelium-dependent contractions in response to acetylcholine, ATP and A 23187 were potentiated significantly in the aorta SHR and were unmasked in that of WKY. However, the contractions were still significantly greater in SHR than in WKY. These contractions were abolished by indomethacin and valeryl salicylate (two cyclo-oxygenase inhibitors) as well as by S 18886 (a TP-receptor antagonist), indicating that the endothelium-dependent contraction produced by the three agonists share the same characteristics. The results of the present study indicate that the release/generation of endotheliumderived contracting factor, requires an increase in endothelial [Ca2+]i.
endothelium-dependent contraction,, endothelium-derived contracting factor,, intracellular concentration of calcium,, spontaneously hypertensive rat
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【期刊论文】A Diffusible Substance(s) Mediates Endothelium-Dependent Contractions in the Aorta of SHR
张寄南, Di Yang, , Michel F
Downloaded from hyper. Ahajournals. Org by on May 9, 2007,-0001,():
-1年11月30日
A modified bioassay system was designed to demonstrate the diffusible nature of endothelium-derived contracting factor(s) released by acetylcholine in the aorta of spontaneously hypertensive rat. In “sandwich”-like layered preparation, isometric tension was recorded from a bioassay strip (without endothelium) in the presence of NG-nitro-L-arginine and tetrahydrobiopterin to selectively potentiate endothelium-dependent contractions. A donor strip (with or without endothelium) was stitched on the bioassay tissue so that it did not directly contribute to the recorded contractions. Acetylcholine induced contractions that occurred only when the donor strip was with endothelium. Superoxide dismutase did not affect but catalase and the combination of superoxide dismutase plus catalase significantly decreased the endothelium-dependent contraction. The contractions in the layered preparations were abolished when the donor strip with endothelium was treated previously with valeryl salicylate, an irreversible cyclooxygenase-1 inhibitor, but remained unaffected when the bioassay strip was treated with the compound. Previous treatment of the bioassay strip alone with S 18886 abolished the contractile response, whereas treatment of the donor strip with endothelium by the selective TP receptor antagonist only produced a moderate inhibition. These results indicate that in the aorta of spontaneously hypertensive rats, endothelium-dependent contractions to acetylcholine involve a diffusible substance(s) released by the endothelium. The production of this contracting factor(s) requires the activation of endothelial cyclooxygenase-1, and its action the activation of TP receptors on the vascular smooth muscle cells.
cyclooxygenase, endothelium-dependent contraction, tetrahydrobiopterin , free radicals, rats,, spontaneously hypertensive, receptors,, thromboxane
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张寄南, Di Yang, , Pascale Gluais, Ji Nan Zhang, Paul M. Vanhoutte, Michel Feletou
J Cardiovasc PharmacolTM ,-0001,():
-1年11月30日
In the aorta of the spontaneously hypertensive rat (SHR), endothelium-dependent contractions are enhanced by inhibitors of NO synthase and scavengers of NO, but not by methylene blue, an inhibitor of guanylyl cyclase, suggesting that the endotheliumderived contracting factor (EDCF) interacts chemically with NO and is inactivated by the latter. However, in view of the relative lack of specificity of methylene blue this hypothesis was re-examined. Acetylcholine-induced endothelium-dependent contractions of isolated rings of SHR aorta were significantly and similarly potentiated by two NOS inhibitors, by two structurally different NO scavengers, by two inhibitors of guanylate cyclase ODQ and NS2028, but to a lesser extent by methylene blue. The contraction of the isolated rat trachea in response to methacholine and the contraction of the rat aorta in response to both 8-isoprostane and KCl were inhibited significantly by methylene blue. Methylene blue binds to the M3 muscarinic receptor subtype but not to the TP receptor. Therefore, methylene blue is an antagonist of the M3 muscarinic receptor subtype, involved in the release of EDCF, and a non-specific inhibitor of TP receptormediated contractions, the receptor involved in the action of EDCF. These inhibitory effects of methylene blue are likely to counteract the effect of the inhibition of soluble guanylate cyclase. These results rule out the hypothesis according to which NO would chemically inactivate EDCF.
EDCF, endothelium-dependent contraction, NO, spontaneously hypertensive rat, guanylate cyclase
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【期刊论文】Control of Glycogen Synthase and Phosphorylase by Amylin in Rat Skeletal Muscle
张寄南, John C. Lawrence, Jr. and Ji-nan Zhang
The Journal of Biological Chemistry Vol. 269, No. 15, Issue of April 15, pp. 11595-11600, 1994,-0001,():
-1年11月30日
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【期刊论文】Insulin Stimulates Dephosphorylation of Phosphorylase in Rat Epitrochlearis Muscles
张寄南, Ji-nan Zhang, Jeffrey Hiken, A lan E. Davis, and JohnC . Lawrence, Jr.
The Journal of Biological Chemistry Vol. 264, No. 29, Issue of October 15, pp. 17513-17523, 1989,-0001,():
-1年11月30日
We have investigated the effects of insulin on the phosphorylation of glycogen phosphorylase in skeletal muscle. Rat epitrochlearis muscles were incubated in vitro with 32Ptio label cellular phosphoproteins, before being treated withho rmones. Phosphorylase, phosphorylase kinase, and glycogen synthase were immunoprecipitated under conditions that prevented changes in their phosphorylation states. Based on measurements of the activity ratio( -AMP/+AMP) and the 32P content of phosphorylase, 4-8% of the phosphorylase in untreated muscles appeared to be phosphorylated. Epinephrine promoted increases of approximately 4-fold in the32P content and activity ratio. Neither these effects nor the epinephrine-stimulated increases in phosphorylation of glycogen synthase andp hosphorylase kinase were attenuated by insulin. However, insulin at physiological concentrations rapidly decreased the 32P content of phosphorylase in muscles incubated without epinephrine. Results from peptide mapping experiments indicate that phosphorylase was phosphorylated at a single site in both control anhdo rmonetreated muscles. The maximum effect of insulin on phosphorylase represented a decrease in32Po f approximately 50%. By comparison, the 32P content of glycogen synthase and the
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张寄南, Di Yang, Michel Fe
British Journal of Pharmacology (2002) 136, 104-110,-0001,():
-1年11月30日
1 Experiments were designed to investigate whether or not oxygen-derived free radicals mediate endothelium-dependent contractions to acetylcholine in the aorta of spontaneously hypertensive rat (SHR). 2 Isometric tension was measured in aortic rings taken from adult male SHR and Wistar-Kyoto rat (WKY) in the presence of NG-nitro-L-arginine. 3 Endothelium-dependent contractions to acetylcholine were signi
Cyclo-oxygenase, endothelium-dependent contractions, endothelium-derived contracting factor(, s), , oxygen-derived free radicals, TP receptor, spontaneously hypertensive rat Abbreviations: DETCA,, diethyldithiocarbamic acid, DMTU,, dimethylthiourea, EDCF,, endothelium-derived contracting factor, SHR,, spontaneously hypertensive rat,
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【期刊论文】Specific Potentiation of Endothelium-Dependent Contractions in SHR by Tetrahydrobiopterin
张寄南, Di Yang, , Nigel Levens, Ji Nan Zhang, Paul M. Vanhoutte, Michel F
Downloaded from hyper. Ahajournals org by on May 9, 2007,-0001,():
-1年11月30日
This study was designed to determine the effect of pteridines, R-and S-tetrahydrobiopterin, sepiapterin, and dihydrobiopterin on endothelium-dependent contractions to acetylcholine in isolated aortas from spontaneously hypertensive rat and normotensive Wistar-Kyoto rat. The noncumulative addition of redox-active pteridines R- and S-tetrahydrobiopterin (but not the oxidized analogues sepiapterin and dihydrobiopterin) produced a concentrationdependent transient contraction in isolated aortic rings from both normotensive and hypertensive rats. R-and S-tetrahydrobiopterin (but not sepiapterin or dihydrobiopterin) potentiated the endothelium-dependent contractions to acetylcholine but only in aortas from hypertensive rats and in the presence of NG-nitro-L-arginine. In these aortas, the generation of oxygen-derived free radicals by the combination of xanthine plus xanthine oxidase also potentiated the endothelium-dependent contractions to acetylcholine. The presence of R-tetrahydrobiopterin did not alter the characteristics of the endothelium-dependent contractions because they were inhibited by valeryl salicylate, an inhibitor of cyclooxygenase-1, by S18886, a TP-receptor antagonist or by Tiron, a cell permeable superoxide anion scavenger. However, the contractions to acetylcholine, which are unaffected by the combination of superoxide dismutase and catalase, become significantly inhibited by these two scavengers in the presence of R-tetrahydrobiopterin. In the presence of NG-nitro-L-arginine, R-tetrahydrobiopterin did not affect the contractions to phenylephrine, U 46619, or to oxygen-derived free radicals generated by xanthine plus xanthine oxidase. These results indicate that the production of superoxide by the autoxidation of tetrahydrobiopterin selectively enhances endothelium-dependent contractions in the spontaneously hypertensive rat when nitric oxide synthase is inhibited.
tetrahydrobiopterin, nitric oxide, endothelium-dependent contractions, rats,, spontaneously hypertensive
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