焦宗宪

焦宗宪，兰州大学基础医学院副教授。

1992--1997 兰州医学院临床医学系本科学习并获医学学士学位。

1997--2000 兰州医学院病理解剖学教研室读研究生并获病理学与病理生理学专业医学硕士学位。

2000--2002 广州医学院病理学教研室任教。

2002--2006 华中科技大学同济医学院病理学系攻读病理学与进病理生理学专业博士研究生并获医学博士学位。

先后在美国Emory大学和Morehouse医学院从事博士后研究工作。

• 中文名称 焦宗宪
• 国籍 中国
• 毕业院校 兰州医学院
• 职业 兰州大学基础医学院副教授

个人简历

　占滑括排许承长物　Resume(including educatio材字蒸称食与额明室n background， English):

　　1992--19来自97 Lanzhou Med图谈个住土末ical College, Lanzhou, Gansu, P. R. China;Degree: Bachelor, Major: Clinical Medicine。

　　1997--2000 Th当宜娘否并威按零何军e Study of the Injury in Alveolar Epithelial Cells Induced by Cigarette Smoke Extract.Degree: Maste伤散款伯频胜育称r, Major: Pathology and Pathophysiology。

　　2000--2002 Teaching assistant, the Departmen360百科t of Pathology, Guangzhou Medical College, Guangzhou, Guangdong, P. R. China;Degree: Ph.D., Major: Pathology and Pathophysiology。

　　2002--伤激服批制乐愿零2006 Tongji Medical College of Huazhong University of Science and Technology, Wuhan, Hubei, P. R. China. Thesis: A Prelimin苦善ary Study on the Location and Expression Level of TGF-β1, TGF-β1 mRNA AND bFGF in Glomerular Fibrotic Diseases。

　　2006--2008 Postdoctoral research fell兵ow, the Department of Pediatrics, Emory U景至niversity School of Medicine,Atlanta,GA,USA.Postdoctoral research fellow, the Cardiovascular Research Institu合克安道整因磁口境试脚te, Morehouse School of Medicine, Atlanta, GA, 引意取西USA。 一、科研方向

　　香烟烟雾提取物致肺泡上皮细胞损伤的分子机制。

　　D活引作建用毛晶NA甲基化在高血压发病机制中的作用。

　　Research Interests:

　　Chronic obstructive pulmonary disease (COPD) is a worldwide leading cause of morbidity and mortality and its prevalence is still 眼rising. It is therefore important to understand the development of this disease in order to develop strategies of prevention, tr呼说源停谈eatment, and cure. Cigarette smoke extract (CSE) is a complex mixture o叶争就原合滑场以件拿f chemicals 证但containing high levels of oxidants and is the major et合孔iologic factor in the devel组层采脸opment of COPD, of which emphysema is a major component. Among the various cell types which compose the lung, the epithelial cells of the alveolar structure appear to be a major target for oxidant injury. It is now well established that type II cells are the stem cells of the alveolar epithelium. After oxidant injury, the rapidity of initiation of type II cell proliferation is crucial for a proper healing. Therefore, characterization of the mechanisms involved in the block of type II cell replication by oxidants and in its reversibility appears to be critical for the understanding and management of many lung diseases associated with oxidative stress. In previous studies, several components of the insulin-like growth factor (IGF) system have been reported involved in the control of proliferation by using a rat type II epithelial cell line, Particularly, accumulation of the IGF binding protein (IGFBP)-2 was associated with block of type II cell proliferation caused by hyperoxia, serum deprivation and glucocorticoid and so on. However the mechanisms regulating human alveolar type II epithelial cell replication upon cigarette smoke exposure remain poorly understood. To provide information on the influence of CSE on the repair capacity of the alveolar epithelium, I am interested in analyzing the effect of CSE on the proliferative response of alveolar type II epithelial cells. To document any protective role of retinoic acid (RA) to reverse the CSE effect, we are to examine the consequence of RA treatment on CSE-induced growth inhibition of type II epithelial cells。

　　Another project is focused on the role of DNA methylation in the pathogenesis of hypertension. Accumulating evidence suggests that key genes become epigenetically repressed during the course of normal development and aging as well as in the course of diseases such as cancer. it is not known whether this mechanism is involved in hypertension. We are intrigued by our preliminary findings that document an up-regulation in expression of DNMT1 during genetic- and angiotensin II (Ang II)-induced hypertension. we specifically hypothesize that DNMT inhibition-mediated demethylation and re-expression of eNOS in no-endothelial cells of the vasculature results in increased production of bioactive NO, increased vasodilation, and lowering of blood pressure。

荣誉称号及奖励

　　曾获兰州医学院1992至1993，1993至1994，1995至1996学年度"三好学生"荣誉称号。1997年获"优秀毕业生"荣誉称号。后被评为1997至1998学年度"优秀研究生"。

　　honors and awards:

　　1992至1993 Triple-A Outstanding Student of Lanzhou Medical College。

　　1993至1994 Triple-A Outstanding Student of Lanzhou Medical College。

　　1995至1996 Triple-A Outstanding Student of Lanzhou Medical College。

　　1997 Excellent Graduate of the Year 1997 of Lanzhou Medical College。

　　1997至1998 Excellent Postgraduate of Lanzhou Medical College。

发表论文(按年度)

　　JIAO Zongxian, AO Qilin, GE Xiaona, XIONG Mi. Cigarette smoke extract inhibits the proliferation of alveolar 来自epithelial cells and augments the expression of p21WAF1. J 础死脱架排古南Huazhong Univ Sci Technolog Med Sci, 2008; 28(1): 6-10。

　　JIAO Zongxian照心粮河川吧头, QU Zhongse创根阶占迅东秋夫如全升n, GE Xiaona, AO Qilin, XIONG Mi. Protective role of tretinoin and N-ace360百科tyl-L-cysteine from antiproliferative action of cigarette smoke extract on alveolar epithelial 染倒证与血试最矿与训cells. Pharmazi水陆每给布诗所沿聚露e, 2007; 62: 539-543。

　　JIAO Zo袁ngxian, AO Qilin, XIONG Mi. Cigarette smoke extract inhibits the pro旧充评liferation of a食防注势单坐政且便lveolar epithelial cells and in飞兰普从显业了站duces apoptosis粮袁待. Acta Physi银整助调ologica Sinica, 2006; 58 (3): 244-254。

　　JIAO Zongxian, GE Xiaona, XIONG Mi. The effect of cigarette smoke extract on the proliferation of alveol令承ar epithelial cells and the expression of p21WAF1. Chinese Journal of Histochemistry And Cytochemistry, 2006; 15 (2):182-189. (in Chine河谈衣降庆功因点se)。

　　JIAO Zongxian. The expressions and effects of TGF-β1 and bFGF in glomerular fib城rosis diseases. Academic Journal of Guangzhou Medical College, 2物王兰001; 29 (1):17-2态上轮丰华引1. (in Chinese)。