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细胞因子与心血管疾病研究室
发布日期:2015-08-27浏览次数: 字号:[ ]

 

 

 

吴立玲     博士 教授
Liling Wu, M.Sc.
Phone:010-82802403
Fax:  010-82802403 
E-mail:pathophy@bjmu.edu.cn

 

教育经历
Education
 
1977      南京铁道医学院医学系   学士
           Medicine, 1973.9-1977.1, Nanjing Railway Medical College China  B.S.
1981      北京医学院病理生理专业 硕士
           Pathophysiology, 1978-1981, Beijing Medical University, China. M.Sc.
 
 
工作经历
Professional Experience
 
2000-present    北京大学医学部 生理学与病理生理学系副主任
      Vice-chairman of Department of Physiology and Pathophysiology, Peking University Health Science  Center, Beijing, China
 
1999-2000      
1993-1994       美国圣路易斯大学医学院做访问学者
1987-1990                      
      Visiting Scholar, Dept. Pharmacological and Physiological Science, St. Louis University Health Science Center USA
 
1995-present    北京大学医学部 生理学与病理生理学系 教授
                Professor of Pathophysiology, Peking University Health Science Center, Beijing, China
 
1990-1995       北京大学医学部 生理学与病理生理学系 副教授
                Associate Professor of Pathophysiology, Beijing Medical University
 
1985-1990       北京大学医学部 生理学与病理生理学系 讲师
                Instructor in Pathophysiology, Beijing Medical University
 
1981-1985       北京大学医学部 生理学与病理生理学系 助教
                Assistant of Pathophysiology, Beijing Medical University
 
2003-2006       北京大学医学部图书馆 馆长
                Director of Peking University Health Science Library
 
研究室成员:
 
李丽,女,副教授,北京大学医学部博士。
王瑾瑜,女,讲师,北京大学医学部博士。
张艳,女,讲师,北京大学医学部博士。
王程,男,讲师,北京大学医学部博士。
向若兰,女,讲师,中国协和医科大学博士。
凡栋:2005级博士生。
丁冲:2006级博士生。
崔晓兵:2007级博士生。
丛馨:2007级博士生。
周允:2004级八年制博士生。
苏运超:2008级博士生。
郭晓红:2009级博士生。
 
研究室概述:
 
本研究室的主要研究方向为心肌肥大时的细胞信号转导通路及脂联素对心脏功能的影响。心肌肥大是心脏对多种机械和生物化学刺激所产生的代偿性反应,同时也是心力衰竭发生的物质基础。心肌肥大会激活细胞内一系列的信号转导通路,它们相互调节,协调作用,共同促进心肌肥大的发生和发展。脂联素是脂肪细胞分泌的一种活性多肽,与2型糖尿病,动脉粥样硬化、心肌肥大等代谢综合症密切相关,是机体一种重要的心血管保护因子。同时,本实验室还与北京大学口腔医学院进行合作,开展家兔正常和移植颌下腺分泌调控机制的研究。
 
具体的研究方向包括:
1、心肌肥大过程中G蛋白与PDGF-β介导的多条信号转导通路之间的交互调节。
2、脂联素在心肌细胞能量代谢中的作用。
3、脂联素对心肌肥大时心肌细胞和成纤维细胞的作用。
4、正常和移植颌下腺中α受体、β受体和Μ受体的分布及其对颌下腺分泌功能的影响。
5、辣椒素对正常和移植颌下腺分泌功能的影响及其机制。
 
Research Description:
The main interest of the laboratory is focused on the signal transduction pathway during cardiac hypertrophy and the effect of adiponectin on cardiac function. Cardiac hypertrophy is not only a compensative response to mechanical and chemic stimulation, but also the basement of heart failure. During cardiac hypertrophy many signal transduction pathways will be activated and contributed to the hypertrophy return. Adiponectin is one kind of peptides which is secreted from adipocytes. It has been proved that adiponectin can regulate metabolism of glucose and fatty acid and the peptide has anti-inflammatory and anti-atherogenic properties. Meanwhile we collaborate with Peking University School of Stomatology to study the regulating mechanism of normal and transferred submandibular gland in rabbit.
 
Our Specific Research Projects Include:
1. The cross-talk between G protein and platelet-derived growth factor-β mediated signal pathway during cardiac hypertrophy.
2. The effect of adiponectin on fatty acid metabolism in heart.
3. The effect of adiponectin on cardiacmyocyte and fibroblast during cardiac hypertrophy.
4. Expression of α、β and Μ receptor and its role in regulating the secretion of normal and transferred submandibular gland.
5. The effect of capsaicin on the secretion of normal and transferred submandibular gland and its  underlying mechanism.

 

Selected Publications (2000-Present):
 
1.  Wang C, Li L, Zhang ZG, Fan D, Zhu Y, Wu LL. Globular adiponectin inhibits angiotensinII-induced nuclear factor κB activation through AMP-activated protein kinase in in cardiac hypertrophy. J Cell Physiol 2009 in press
 
2.  Li YM, Zhang Y, Shi L, Xiang B, Cong X, Zhang YY, Wu LL, Yu GY. Isoproterenol improves secretion of transplanted submandibular gland. J Dent Res 2009 88(5):477-482.
 
3.  Bin X, Zhang Y, Li YM, Gao Y, Gan YH, Wu LL, Yu GY. Phenylephrine protects autotransplanted rabbit submandibular gland from apoptosis.Biochem Biophys Res Commun 2008; 377 (1) 210–214.
 
4.  Wang C, Wu LL, Liu J, Zhang ZG, Fan D, Li L. The crosstalk between angiotensin II- and platelet-derived growth factor-BB mediated signal pathways in cardiomyocytes. Chin Med J 2008; 121(3):236-240.
 
5.  Li L, Wu LL, Wang C, Liu LM, Zhao YL. Adiponectin modulates carnitine palmitoyltransferase-1 through AMPK signaling cascade in rat cardiomyocytes. Regulatory Peptides 2007;139:72–79.
 
6.  Li YM, Zhang Y, Xiang B, Zhang YY, Wu LL, Yu GY. Expression and functional analysis of β-adrenoceptor subtypes in rabbit submandibular gland. Life Sciences 2006, 79:2091-2098.
 
7.  Huang Z, Wu LL, Zhang YY, Gao Y, Yu GY. Functional α1-adrenoceptor subtypes in human submandibular glands. J Dent Res 2006;85(3):251-256.
 
8.  Zhang Y, Xiang B, Li YM, Wang Y, Wang X, Wang YN, Wu LL, Yu GY. Expression and characteristics of vanilloid receptor 1 in the rabbit submandibular gland. Biochem Biophys Res Commun 2006;345:467–473.
 
9.  Liu J, Wu LL, Li L, Zhang L, Song ZE. Growth-promoting effect of platelet-derived growth factor on rat cardiac myocytes. Regulatory Peptides 2005,127:11-18.
 
10. Zhao YL, Liu J, Li L, Liu LM, Wu LL. Role of Ras/PKC-zeta/MEK/ERK1/2 Signaling Pathway in Angiotensin II Induced Vascular Smooth Muscle Cell Proliferation. Regulatory Peptides 2005, 128:43-50.
 
11. Bai H, Wu LL, Xing DQ, Liu J, Zhao YL. Angiotensin Ⅱ induced upregulation of Gaq/11, phospholipase C b3 and extracellular signal-regulated kinase 1/2 via angiotensin Ⅱ type 1 receptor. Chinese Medical Journal 2004, 117(1):88-93.
 
12. Wu LL, Yang SL, Yang RC, et al. G protein and adenylate cyclase complex-mediated signal transduction in the rat heart during sepsis. Shock, 2003,19(6) 533-537.
 
13. Wu LL, Tang CS, Dong LW, Liu MS. Altered phospholamban-calcium ATPase interaction in cardiac sarcoplasmic reticulum during the progression of sepsis. Shock. 2002, 17(5):389-393.
 
14. Xing DQ, Bai H, Zhao YL, Wu LL. Regulation of angiotensinⅡon Gαq/11 protein of vascular smooth muscle cell and its underlying mechanism. Chinese Science Bulletin 2002, 47(16): 1369-1372.
 
15. Bai H, Sun YP, Xing DQ, Liu J, Wu LL. Platelet-derived growth factor receptor-β in myocyte was upregulated by angiotensin II. Chinese Science Bulletin. 2002, 47(12):1015-1018.
 
16. Bai H, Sun YP, Xing DQ, Liu J, Wu LL. Angiotensin Ⅱ up-regulates platelet-derived growth factor receptor β in rat cardiocytes. Chinese Science Bulletin 2001, 46(17):1450.
 
17. Wu LL, Ji Y, Dong LW, et al. Calcium uptake by sarcoplasmic reticulum is impaired during the hypodynamic phase of sepsis in the rat heart. Shock 2001,15(1):49.
 
18. Dong LW, Wu LL, Ji Y, et al. Impairment of the ryanodine-sensitive calcium release channels in the cardiac sarcoplasmic reticulum and its underlying mechanism during the hypodynamic phase of sepsis. Shock 2001, 16(1):33.
 
19. Wu LL,Dong LW, Liu MS. Alterations of G-protein and adenylate cyclase signaling in rat liver during the progression of sepsis. Shock 1999;11(1)39-43
 
20. Tang CS, Yang J, Wu LL,Dong LW, Liu MS. Phosphorylation of β-adrenergic receptor leads to its redistribution in rat heart during sepsis. Am J Physiol 1998;274:R1078-R1086
 
21. Ji Y, Ren XY, Zhao YT, Dong LW, Wu LL, Su JY. Role of intracardiac angiotensin II in cardiac dysfunction of rat during septic shock. Chinese medical journal 1996, 109:864-867
 
22. Wu LL, Liu MS. Heart sarcolemmal Ca2+ transport in endotoxin shock:: I impairment of ATP-dependent Ca2+ transport. Mol Cell Biochem 1992, 112:125-133
 
23. Liu MS, Wu LL. Heart sarcolemmal Ca2+ transport in endotoxin shock::II. Mechanism of impairment in ATP-dependent Ca2+ transport. Mol and Cell Biochem 1992, 112:135-14.
 
24. Wu LL, Liu MS. Altered ryanodine receptor of canine cardiac sarcoplasmic rericulum and its underlying mechanism in endotoxin shock. J Surg Res 1992, 53:82-90
 
25. Liu MS, Wu LL. Reduction in the Ca2+ induced Ca2+ release from canine cardiac sarcoplasmic reticulum following endotoxin administration. Biochem. Biophy. Res Communi. 1991, 174:1248-1254
 
26. Wu LL, Liu MS. Impaired calcium uptake by cardiac sarcoplasmic reticulum and its underlying mechanism in endotoxin shock. Mol Cell Biochem 1991, 108:9-17.




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