王国平
心血管病理学和分子病理学
个性化签名
- 姓名:王国平
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学术头衔:
博士生导师
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学科领域:
病理学
- 研究兴趣:心血管病理学和分子病理学
王国平,教授,博士生导师,华中科技大学同济医学院病理学系系主任,附属同济医院病理研究所所长兼病理科主任,湖北省医学会病理学分会主任委员,中国医师协会病理科医师分会常务委员。1982至1987年,就读于湖北医学院咸宁分院医学系,毕业后获医学学士学位并留校任病理学助教;1989至1996年于同济医科大学病理学系攻读硕士和博士学位,毕业后留校任病理学讲师;博士论文于1997年全文发表在国际动脉粥样硬化协会会刊ATHEROSCLEROSIS上,并于1998年获湖北省首届优秀博士论文奖,同年入选同济医科大学“211人才工程--学术和技术带头人” ,2002年获湖北省自然科学三等奖。1998年至2004年先后在日本国立熊本大学医学院、香港大学医学院和加拿大西安大略大学医学院分别任访问学者、博士后研究员和研究员;2004年回华中科技大学同济医学院工作,任病理学系教授,2004年入选教育部新世纪优秀人才支持计划、华中科技大学博士生导师、《临床与实验病理学杂志》编委、《中华病理学杂志》特邀审稿专家。曾先后在国内外重要学术期刊上发表论文30余篇,其中被SCI收录9篇,并于2005年被邀请在Experimental Biology 2005上作大会发言。至目前为止,主要论文被引用次数达200人次。目前主要从事病理学系的各级教学、科研及临床病理诊断工作。主要的研究方向为心血管病理学和分子病理学,其科研工作的中心任务是运用现代分子病理学的思维和技术,探讨心血管疾病的发生发展规律及其治疗措施,尤其是干细胞在心血管疾病修复过程中的作用。
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成果数
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王国平, Guoping WANG, Yaw L. SIOW and Karmin O
,-0001,():
-1年11月30日
Monocyte chemoattractant protein-1 (MCP-1) is a potent chemokine that stimulates the migration of monocytes into the intima of arterial walls. Although many factors that induce MCP-1 expression have been identi
atherosclerosis,, calcium,, IjBa,, oxidative stress,, phosphorylation.,
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王国平, WANG Guoping, DENG Zhongduan and NI Juan
Chinese Medical Journal 2000; 113 (7): 667-669,-0001,():
-1年11月30日
Objective To understand the role of oxidized low density lipoprotein (OX-LDL) in the pathogenesis of thrombotic complications in atherogenesis. Methods Low density lipoprotein was isolated from normal heparinized bleed by density gradient ultracentrifugation and oxidized by CuCl2. Total RNA was extracted from human umbilical vein endothelial cells (HUVECs) exposed to LDL or OX-LDL, using the guanidinium isothiocyanate method. The quantification of tissue factor pathway inhibitor (TFPI) mRNA in HUVECs was carried out by reverse transcriptase-polymerase chain reaction (RT-PCR). Results HUVECs were able to express TFPI mRNA constitutively. The expression was not affected by LDL but was effectively inhibited by OX-LDL in a time-and dose-dependent manner. Conclusions The results suggest that oxidized LDL may play an important role in inducing coagulation in atherosclerotic lesions by the inhibition of expression of TFPI in vascular endothelial cells.
tissue factor pathway inhibitor
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王国平, Guo-Ping Wang*, Zhong-Duan Deng, Juan Ni, Zhi-Ling Qu
G.-P. Wang et al./Atherosclerosis 133(1997)31-36,-0001,():
-1年11月30日
The migration of monocytes into arterial subendothelial space is one of the earliest events in atherogenesis. Monocyte chemoattractant protein 1 (MCP-1) is a potent monocyte chemoattractant. The purpose of this work was to examine whether oxidized low density lipoprotein (OX-LDL) and very low density lipoprotein (OX-VLDL) have any effect on the expression of MCP-1 mRNA and protein in rabbit peritoneal exudate macrophages. The total RNA was extracted from the macrophages after 24 h exposure to LDL, VLDL, OX-LDL, and OX-VLDL, respectively, and the media (LDL-CM, VLDL-CM, OX-LDL-CM and OX-VLDL-CM) conditioned by the macrophages exposed to the above-mentioned lipoproteins were collected. The MCP-1 mRNA expression in macrophages was examined by Northern blot analysis. Meanwhile, MCP-1 protein in the conditioned media was determined by sandwich ELISA. The chemotactic activity of the conditioned media for monocytes was determined by micropore filter assay. The results revealed that the macrophages can express MCP-1, and 24h exposure to OX-LDL and OX-VLDL induced a 3.2-fold and a 3.4-fold increase in MCP-1 mRNA expression in macrophages and a 2.2-fold and a 2.5-fold increase in the level of MCP-1 protein in the conditioned media, respectively. However, 24h exposure to LDL and VLDL only induced a slight increase in the expression of MCP-1 mRNA and protein in macrophages. Furthermore, the migration distance of monocyte induced by OX-LDL-CM and OX-VLDL-CM was longer than that induced by LDL-CM and VLDL-CM, as well as by CM. We conclude that the macrophages can express MCP-1, and OX-LDL and OX- VLDL induce stronger MCP-1 expression. It suggests that macrophages may amplify the recruitment of monocytes into subendothelial space, and OX-LDL and OX-VLDL may play an important role in the pathogenesis of atherosclerosis through enhancing the MCP-1 expression in macrophages.
LDL, VLDL, Oxidation, MCP-1, Macrophage, Atherosclerosis
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王国平, GUOPING WANG, YAW L. SIOW, AND KARMIN O
Am J Physiol Heart Circ Physiol 280: H2840-H2847, 2001.,-0001,():
-1年11月30日
Wang, Guoping, Yaw L. Siow, and Karmin O.Homocysteine induces monocyte chemoattractant protein-1 expression by activating NF-kB in THP-1 macrophages. Am J Physiol Heart Circ Physiol 280: H2840-H2847, 2001.-Homocysteinemia is an independent risk factor for cardiovascular disorders. The recruitment of monocytes is an important event in atherogenesis. Monocyte chemoattractant protein-1 (MCP-1) is a potent chemokine that stimulates monocyte migration into the intima of arterial walls. The objective of the present study was to investigate the effect of homocysteine on MCP-1 expression in macrophages and the underlying mechanism of such effect. Human monocytic cell (THP-1)-derived macrophages were incubated with homocysteine. By nuclease protection assay and ELISA, homocysteine (0.05-0.2mM) was shown to significantly enhance the expression of MCP-1 mRNA (up to 2.6-fold) and protein (up to 4.8-fold) in these cells. Homocysteine-induced MCP-1 expression resulted in increased monocyte chemotaxis. The increase in MCP-1 expression was associated with activation of nuclear factor (NF)-kB due to increased phosphorylation of the inhibitory protein (IkB-a) as well as reduced expression of IkB-a mRNA in homocysteine-treated cells. In conclusion, our results demonstrate that homocysteine, at pathological concentration, stimulates MCP-1 expression in THP-1 macrophages via NF-kB activation.
chemotaxis, inhibitory protein, IkB-a, atherosclerosis, nuclear factor-kB
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王国平, Guoping WANG and Karmin O
Biochem. J. (2001) 357, 233-240,-0001,():
-1年11月30日
Homocysteinaemia is an independent risk factor for atherosclerosis. The development of atherosclerosis involves monocyte chemoattractant protein 1 (MCP-1)-mediated monocyte recruitment to the lesion site. The action of MCP-1 is mostly via its interaction with MCP-1 receptor (CCR2), which is the major receptor for MCP-1 on the surface of monocytes. The objective of the present study was to investigate the e
atherosclerosis,, chemotaxis,, oxidative stress,, superoxide.,
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王国平, Guoping Wang, * Connie W. H. Woo, * Fion L. Sung, Yaw L. Siow, Karmin O
Arterioscler Thromb Vasc Biol. November 2002,-0001,():
-1年11月30日
Objective-The stimulatory effect of homocysteine (Hcy) on monocyte chemoattractant protein (MCP)-1 expression in vitro has been suggested to play an important role in Hcy-mediated atherosclerosis. We investigated whether such a stimulatory effect occurs in vivo, leading to monocyte adhesion to the endothelium. Methods and Results-Sprague-Dawley rats were divided into 4 groups. Hyperhomocysteinemia was induced in 1 group of rats after 4 weeks of a high-methionine diet (serum Hcy levels were 4-to 5-fold higher than levels in control rats). The number of ED-1–positive cells present on the surface of aortic endothelium was significantly elevated in hyperhomocysteinemic rats. There was a significant increase in the expression of MCP-1, vascular cell adhesion molecule-1 (VCAM-1), and E-selectin in the endothelium. Antibodies recognizing MCP-1, VCAM-1, or E-selectin could abolish the enhanced monocyte binding to the aortic endothelium of hyperhomocysteinemic rats. Endotheliumdependent aortic relaxation was impaired in hyperhomocysteinemic rats. Conclusions-These results suggest that in the absence of other known risk factors, hyperhomocysteinemia stimulates the expression of MCP-1, VCAM-1, and E-selectin in vivo, leading to increased monocyte adhesion to the aortic endothelium. Such an effect may contribute significantly to the development of atherosclerosis by facilitating monocyte/macrophage infiltration into the arterial wall. (Arterioscler Thromb Vasc Biol. 2002; 22: 1777-1783.)
hyperhomocysteinemia ■ atherosclerosis ■ monocyte chemoattractant protein-1 ■ cytokines ■ monocytes
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