1.个人简介
Email: hanyp@scu.edu.cn or southcalyph@yahoo.com
四川大学，生命科学学院
韩源平 (Yuan-Ping Han，Ph.D.) 博士，在美国学习工作二十多年后，作为海外人才引进人才回到母校四川大学，现任生命科学学院教授，美国Cedars-Sinai Medical Center客座教授。研究领域主要在肝硬化，脂肪肝，代谢综合症发生的整和生理／病理学。作为美国南加州大学(University of Southern California， USC，Keck School of Medicine) 博士导师, 他的研究得到National Institutes of Health（NIH）多个基金的支持, 包括两个5年R01基金, 共$2.7 million以及其它基金。在四川大学的4年期间，在四川大学／985启动基金的支持下，他获得了国家自然基金，四川省科技厅科技支撑，以及制药公司开的开发基金。他是美国NIH, NSF, 欧洲Wellcome Foundation的基金评委。为多个专业期刊, 如Hepatology, Am J Pathology, J Biological Chemistry, J of Immunology审稿。在肝脏方面, 主要从事肝星状细胞及肝硬化，以及脂肪肝（NASH）的机理研究。他呈经在制药领域（GSK，葛兰素史克研发总部,以及四川抗生素研究所）从事新药物的开发研究。在美国期间长期为制药公司担任顾问(consultant)。研究方法涉及分子生物学，生物化学，组织及细胞生物学，免疫学，人体生理，病理学的整合，以及转化及临床应用。除了基础研究，我们也开展针对脂肪肝(NASH)／代谢综合征，以及抗肝硬化新药的研发。
回到川大3年来建立了实验室以及动物房，有10位研究生，我们获得了国家自然基金，四川省科技厅的支撑基金，中国肝病防治学会的研究基金，以及制药厂的开发基金。在教学方面，主持全英语生物化学课程。同时，我们与美国Cedars-Sinai Medical Center 以及南加州大学（USC）开展合作，对研究生采用双导师制度。
2.教育经历
?1978-1982, 四川大学, 生物系, 主修生物化学, 学士学位
?1990-1996, 西奈山医学院 (The Mount Sinai School of Medicine, New York), 主修生物医学科学（Biomedical Science）, 获博士学位 ，Ph.D. 导师, Dr. Ronald A. Kohanski
?1996-1999, 南加大洛杉矶儿童医院Los Angeles Children’s Hospital/University of Southern California, 博士后 (1996-1999), 导师, Dr. Yun-Kai (Teddy) Fong
3.研究工作经历
?1982-1985, 地质矿产部工艺研究所, 助理研究员
?1985-1989, 四川抗菌素研究所, 助理研究员
?1989-1990, SmithKline Pharmaceuticals (葛兰素史克, 美国, 费城), 从事新药发现研究
?2000-2003, 南加州大学 University of Southern California, Keck School of Medicine, 助理研究员
?2004-2011, 南加州大学 University of Southern California, Keck School of Medicine, 助理教授 (Assistant Professor at Tenure Track)。 USC Keck School of Medicine, PIBBS 博士研究生导师。
?2004年-现在，南加州大学，Keck School of Medicine, 酒精肝病及胰腺疾病研究中心会员
?2011-至今首都医科大学，北京佑安医院客座教授
?2012-至今，Cedars-Sinai Medical Center (Los Angeles), 客座教授，项目合作。
?2012-至今, 四川大学，生命科学学院，教授。
4.期刊评审
Journal of Clinical Investigation
Hepatology
American Journal of Pathology
American Journal of Physiology (Gastrointestinal and Liver Physiology)
Wound Repair and Regeneration Journal
Journal of Biological Chemistry
Life Science Journal
Journal of the National Cancer Institute
Journal of Cellular and Molecular Medicine
5. 基金评审
National Science Foundation (NSF)
Wellcome Foundation
National Institutes of Health (NIH)
中国自然基金
6.研究基金
1. Principal Investigator: “ACT, a pathophysiological inhibitor of MMP-9 Activation”.
R01, AR051558, NIAMS, 7/1/2004-6/30/2009
The goal of this grant is to identify and characterize alpha-ACT as a novel inhibitor controlling proMMP9 conversion in human skin.
2. Principal Investigator: “Hepatic Stellate Cell Derived MMP9 in Liver Fibrogenesis”.
R01, DK069418, NIDDK, 9/1/2004-8/30/2009
The major goal of this grant is to elucidate the mechanism of fibrogenic activation of hepatic stellate cells, an essential process in liver fibrogenesis. Specifically, we have addressed the role of IL-1 in ECM remodeling and activation of hepatic stellate cells.
3. Pilot Project Investigator: “Cytokine regulation of MMPs and TIMPs by alcoholic liver”. 5P50AA011999, Pilot Project Grant, NIAAA, 12/30/2002-12/31/2004， The aims of this pilot project are to explore the roles of MMPs in hepatic stellate cell activation (trans-differentiation) and the inflammation mediated regulation of MMPs.
4. Principal Investigator: “Purification of the hepatic stellate cell produced proMMP-9 activator”
Robert E. and May R. Wright Foundation (II), 6/30/2004-6/30/2006 We recently demonstrated that IL-1a induced MMP-9 has an essential role in trans-differentiation of hepatic stellate cells. However, an outstanding question is that how proMMP-9 is converted into active form by hepatic stellate cells. This grant will support us to identify this activator through protein biochemical and genomic approaches. 5. Principal Investigator: “Identification of the Cellular Factors
Controlling MMP-9 Activation in Human Skin and Implication in Cancer Metastasis”. Robert E. and May R. Wright Foundation (I), 7/1/2002-6/30/2004
The aim of this project is to purify the putative proMMP-9 activator from human skin. Through the original work we have 1) defined the cytokine regulation of proMMP-9 activation by human skin, 2) established a protocol to extract the activator and 3) characterized the putative activator as a tissue bound chymotrypsin-like proteinase.
6. Principal Investigator: “The cellular factors promote MMP-9 activation in chronic wound". The Plastic Surgery Education Foundation, PI, 2000-2001 The aim of this grant is to understand the cytokine mediated induction of proMMP-9 expression by dermal fibroblasts and keratinocytes. The signal transduction leading expression MMP is the key emphasis.
7. Principal Investigator “Regulatory T cells in liver injury and fibrosis”.
Pilot Grant, NIDDK, issued by the Research Center of Liver Diseases. 3/15/2010-6/13/2011
8. 四川大学，海外人才引进计划及985计划，
启动基金： ￥ 800,000
2012／9/1 – 2016／9/1
9. 中国肝炎防治基金会王宝恩肝纤维化研究基金
“调节性T－细胞在重度肝纤维化及肝硬化中的关键作用”。
￥ 50,000，2014/5/1 － 2015/5/1.
10. 四川省科技支撑计划项目
“脂肪性肝炎发生的系统生物学及抗脂肪肝的新疗法”**188
￥ 200,000；2014/11/13 － 2016/11/13
11. 成都通德制药公司
“对通德制药公司现有药物的二次开发”
￥ 650,000；2014/11/20 － 2016/11/20
12. 中国自然基金
“维生素D调节肠道抗菌肽及菌群，以低于代谢综合症”。#**￥ 748,000：2016／01 － 2019/12.
7、研究领域及成果。
(1) 代谢综合症，脂肪肝的机理及新疗法的开发。
近年来我们将工作的重点的一部分转移到代谢综合症，脂肪肝，肥胖的机理研究及新药物的开发。随着社会经济的巨大发展，代谢综合症（Metabolic Syndrome，MS) 表现为高血脂，脂肪肝，肥胖，糖尿病，呈蔓延之势。近来官方的统计，中国有1亿六千****群患有不同程度的代谢综合症。在西方，四分之一的成人为肥胖。代谢综合症的危险性在于引发糖尿病，心血管疾病，及脑中风，已成为最主要的死亡杀手。代谢综合症的发生与高糖，高脂肪饮食有密切关系。改善饮食及生活方式是治疗代谢综合症的有效方法。在药物治疗方法，降胆固醇，降高血压，降血糖是主要的策略。另外，使异位的脂肪（腹内）回归到脂肪皮下细胞，也是防治代谢综合症的新方向。基于多年来我们在慢性疾病研究的经验，我们采用系统生物学的方法，从新的角度及方法来研究代谢综合症。代谢综合症的发生分为三个阶段。第一步，高脂肪，高果糖饮食引起的肠道菌群(microbiota)的改变，造成血液内毒素的上升及腹部脂肪组织的慢性炎症。第二步，慢性炎症造成胰岛素抵抗，糖耐受，II型糖尿病。作为弥补机制，高血糖在肝脏转化为脂肪酸，形成高血脂，脂肪肝。而脂肪肝及腹内脂肪产生的炎症会造成肝脏损伤，导致高密度脂蛋白（HDL）下降，凝血机制增强。第三步，持续的糖尿病，高血脂，凝血异常，将产生心血管阻塞，中风，加速死亡。为此，我们以系统生物学的方法，发现高脂肪饮食及维生素D缺乏诱导肠道菌群的改变，Paneth细胞抗菌多肽的下降，肠道及腹内脂肪，胰腺的低度炎症，造成胰岛素抵抗，产生脂肪肝，糖耐受。以此模型， 我们将阐述代谢综合症的发生机理。同时，我们正在研究开发全新的药物，用于代谢综合症的预防及治疗。
（2）组织纤维化的细胞生物学。
在美国南加大（University of Southern California)工作期间，作为PI并在两个NIH R01基金的资助下，我们长期从事这方面的研究。广义的组织损伤包括病毒感染，污染毒物的摄入，及多种慢性疾病，肿瘤等等。损伤以后，肌体有两种选择，是再生，还是修复。大多数的组织仅有极小的再生能力（例如肝脏，皮肤）。而采用修复是大规模或是持续损伤的首要选择。修复的主要特征是产生纤维化的组织结构。作为进化的选择结果，组织纤维化对于肌体是有益的，它为失去的组织打上了“补丁”，否则因失去的组织，个体不能幸存。但是，持续的纤维化将使得慢性疾病，例如肿瘤得以持续。器官的老年衰竭也是组织纤维化的结果。据估计，大约50%的死亡都与组织纤维化有关。大多数的肿瘤之所以能够持续的原因，在很大程度上是因为纤维化组织为肿瘤提供了生长的环境。我们的工作主要集中于肝星状细胞 (hepatic stellate cells) 的转分化（trans-differentiation)。我们发现在肝星状细胞转分化过程中，多个MMP基因被不可逆地关闭，消静（silencing）。我们认为，在正常肝血窦中星状细胞的表型是有其3维ECM通过表观遗传（epigenetic control) 所决定的。更进一步，根据我们的发现，我们认为3D ECM通过下调II－型HDAC，使MMP基因群（mmp loci) 处于表观遗传水平的开放状态，在炎症因子引发的信号传导下，能够大量表达，释放生长因子，开启损伤及修复。星状细胞在生长因子的促动下转化为肌成纤维母细胞（myofibroblasts), 并形成纤维组织。MMP基因在肌成纤维母细胞的消静，将促进ECM的积累以及纤维化。我们发现，在星状细胞转分化过程中，II－型HDAC趋于上升，蛋白质稳定，导致MMP基因被抑制。我们将继续回答以下问题：（1）MMP基因群的表观遗传景观在转分化过程中的改变，从开放到抑制？（2）II－型HDAC的降解酶，以及在纤维化中的作用？（3）3D ECM对II－型HDAC的调控以及在损伤中MMP基因的表达。
（3）肝纤维化中的免疫耐受。
肝纤维化不但是由于星状细胞的转分化及肌纤维母细胞的形成，同样重要的是肝硬化所处的免疫赖受的宏观环境（macro-environment of immune tolerance），使得纤维组织免于被清除，逃逸免疫监控 (escaping from immune surveillance)。同时，免疫赖受也为肿瘤生长，转移，恶化提供环境条件。在前期工作中，我们发现天然调节性T细胞（naturally occurring Tregs, nTres) 在肝损伤中的下降是由于其细胞凋亡所致，而在肝修复过程中产生的诱导型Tregs（induced Tregs， iTregs）是由于MMP激活的TGF－beta从而诱道Foxp3所致。该工作近来被Journal of Molecular Cell Biology (影响因子: 7.3) 接受。我们发现伴随肝纤维化的形成，Tregs聚集于纤维桥附近，说明Tregs产生的免疫赖受可能促进纤维化的持续。当我们用单抗干预Tregs时，发现能够促进小鼠肝硬化的消融，表明Tregs可能抑制纤维的消融。我们发现Tregs通过上调TIMP来抑制MMP。同时，我们在肝硬化病人的肝组织中检出Tregs的升高，说明可能的因果关系。为此，我们提出新的假设：肝星状细胞所释放的MMP通过激活TGF－beta，并且在IL－1作用下释放维甲酸（retinoic acid）来诱导Tregs，使纤维化免于被清除。另一方面，与北京佑安医院合作，我们也对II－型巨噬细胞（alternatively activated macrophages) 在纤维化的免疫耐受开展了大量工作。
8. 发表的文章。
Peer-Reviewed
1. Yuan-Ping Han, Kohanski RA.
“Phenylarsine oxide inhibits insulin activation of phosphatidylinositol 3'-kinase”.
Biochem Biophys Res Commun 1997 Oct 9;239 (1):316-21.
2. Frankel M, Bishop SM, Ablooglu AJ, Yuan-Ping Han, Kohanski RA. “Conformational changes in the activation loop of the insulin receptor's kinase domain”.
Protein Science 1999 Oct; 8(10): 2158-65.
3. Yuan-Ping Han, Tuan TL, Wu H, Hughes M, Garner WL.
“TNF-alpha stimulates activation of pro-MMP2 in human skin through NF-kappa B mediated induction of MT1-MMP”.
Journal of Cell Science 2001; 114(Pt 1):131-139.
4. Yuan-Ping Han, Tai-Lan Tuan, Huayang Wu, Michael Hughes, Warren L. Garner. “TGF-beta and TNF-alpha mediated induction and proteolytic activation of MMP-9 in human skin”.
Journal of Biological Chemistry. 2001, vol.276 (25); 22341-22350.
5. Yuan-Ping Han, Micheal W. Hughes, Yih-Dar Nien and Warren L. Garner.
“IL-8-Stimulated Expression of Urokinase-Type Plasminogen Activator in Human Skin and Human Epidermal Cells”.
Journal of Surgery Research. 2002 Aug;106(2):328.
6. Mei Chen, Fritz K. Costa, Christopher R. Lindvay, Yuan-Ping Han, and David T. Woodley.
“The Recombinant Expression of Full-length Type VII Collagen and
Characterization of Molecular Mechanisms Underlying Dystrophic Epidermolysis
Bullosa”.
Journal of Biological Chemistry. 2002, vol. 277: 2118-2124.
7. Yuan-Ping Han, Yih-Dar Nien and Warren L.Garner.
“Recombinant human platelet-derived growth factor and transforming growth factor-beta mediated contraction of human dermal fibroblast populated lattices is inhibited by Rho/GTPase inhibitor but not require phosphatidylinositol-3’ kinase”.
Wound Repair and Regeneration. 2002, vol. 10, 169-176.
8. Yuan-Ping Han*, Yih-Dar Nien and Warren L.Garner.
“TNF-alpha mediated proteolytic activation of pro-MMP-9 in human skin is controlled by down regulation of the tissue inhibitor, TIMP-1 and mediated by tissue bound chymotrypsin-like proteinase”.
Journal of Biological Chemistry. 2002, 277: 27319-27327.
9. Yuan-Ping Han, Yih-Dar Nien and Warren L.Garner.
“Fibrinogen inhibits fibroblast-mediated contraction of collagen”.
Wound Repair and Regeneration. 2003 Sep;11(5):380-385.
10. Yuan-Ping Han*, Ling Zhou, Jiaohong Wang, Shigang Xiong, Warren L. Garner, Samuel W. French, Hidekazu Tsukamoto.
“Essential role of matrix metalloproteinases in interleukin-1 induced myofibrobalstic activation of hepatic stellate cell in collagen”.
Journal of Biological Chemistry. 2004, vol. 279, 4820-4828
11. Yuan-Ping Han, Downey S and Warren L.Garner.
“Interleukin-1alpha-induced proteolytic activation of metalloproteinase-9 by human skin”.
Surgery. 2005 Nov;138(5):932-9.
12. Yuan-Ping Han*.
“Matrix metalloproteinases, the pros and cons, in liver fibrosis”.
Journal of Gastroenterology & Hepatology. 2006 Oct; 21 Suppl 3:S88-91.
13. Yuan-Ping Han*, Chunli Yan, Ling Zhou, Lan Qin, and Hidekazu Tsukamoto.
“A Matrix Metalloproteinase-9 Activation Cascade by Hepatic Stellate Cells in Trans-differentiation in the hree-dimensional Extracellular Matrix”.
Journal of Biological Chemistry. 2007 Apr 27;282(17):12928-39
14. Goldberg MT, Han YP, Yan C, Shaw MC, Garner WL.
“TNF-alpha Suppresses alpha-Smooth Muscle Actin Expression in Human Dermal Fibroblasts: An Implication for Abnormal Wound Healing”.
Journal of Investigative Dermatology. 2007 May 31;127 (11):2645-55
15.Cheng JH, She H, Han YP, Wang J, Xiong S, Asahina K, Tsukamoto H.
“Wnt antagonism inhibits hepatic stellate cell activation and liver fibrosis”.
American Journal of Physiololy, (Gastrointest Liver Physiol) 2007, Nov 15; [Epub ahead of print] PMID: **
16. Yuan-Ping Han*, Chunli Yan and Warren L Garner.
“Proteolytic Activation of Matrix Metalloproteinase-9 in Skin Wound Healing Is Inhibited by alpha-1-Antichymotrypsin”.
Journal of Investigative Dermatology. 2008 September; 128(9): 2334–2342.
17. Chunli Yan, Ling Zhou, and Yuan-Ping Han*.
“Contribution of hepatic stellate cells and matrix metalloproteinase-9 in acute liver failure”.
Liver International. 2008 May 26. [Epub ahead of print].
18. Cheng CF, Fan J, Fedesco M, Guan S, Li Y, Bandyopadhyay B, Birght AM, Yerushalmi D, Liang M, Chen, Han YP, Woodley DT, Li W.
“Transforming growth factor alpha (TGFalpha)-stimulated secretion of HSP90alpha: using the receptor LRP-1/CD91 to promote human skin cell migration against a TGFbeta-rich environment during wound healing”.
Molecular Cell Biolology. 2008 May;28(10):3344-58. Epub 2008 Mar 10, MID:**.
19. Ling Zhou, Chunli Yan, Wei Li, Yujiro Kida, Warren L. Garner and Yuan-Ping Han*.
“p21 activated kinase (PAK) controls expression of MMP-9”.
BMC Immunology 2009, 10:15,19 March
20. Roben L. Gieling, Wallace, K. and Yuan-Ping Han*
“Participation of Interleukin-1 in Liver Injury induced Fibrosis”.
American Journal of Physiology, (Gastrointest Liver Physiol) . 2009, vol. 296,1324-31
21. MJ Reiss, Yuan-Ping Han, E Garcia, YK Hong, and WL Garner.
“ 1-Antichymotrypsin activity correlates with and may modulate matrix metalloproteinase-9 in human acute wounds ”.
Wound Healing and Regeneration, 2009, Published Online: May 20 2009, p 418-426
22. Shengwen Calvin Li, Yuan-Ping Han, Brent A. Dethlefs and William Gunter Loudon.
“Therapeutic Window of Stem Cell Potential for Targeting Pediatric Malignant Brain Tumor: An Opportunity for Stem Cell Therapy”.
Stem Cell Review and Reports, 2009, vol.5, issue 4, p446
23. MJ Reiss, Yuan-Ping Han, E Garcia, YK Hong, and WL Garner.
“Excessive Amount of Matrix Metalloproteinase-9 Delays Wound Healing in a Murine Wound Model”.
Surgery, 2010, February, Volume 147, Issue 2, Pages 295-302
24. Keigo Machida, Hidekazu Tsukamoto, Jian-Chang Liu, Yuan-Ping Han, Sugantha Govindarajan, Michael Lai, Shizuo Akira, James Ou, “c-Jun mediates HCV hepatocarcinogenesis through STAT3 and nitric oxide-dependent impairment of oxidative DNA repair”.
Hepatology, 2010 Aug;52(2):480-92
25. Chunli Yang, Wesley Grimm, Warren Garner, and Yuan-Ping Han*,
“Tumor necrosis factor-alpha induced epithelial-to-mesencymal transition in human skin fibrogenesis is mediated by bone morphogenetin protein-2”.
American Journal of Pathology, 2010, May. 176: 2247-2258. (Cover story)
26. Lan Qin and Yuan-Ping Han*.
“Epigenetic Repression of Matrix Metalloproteinases in Myofibroblastic Hepatic Stellate Cells through Histone Deacetylases 4,Implication in Tissue Fibrosis ”.
American Journal of Pathology, 2010, volume 177, Issue 4, page 1915 (Monthly Highlight)
27. Xiaohui Zhou, Zanxian Xia, Qin Lan, Julie Wang, Wenru Su,Yuan-Ping Han, Huimin Fan, Zhongmin Liu, William Stohl, and Song Guo Zheng.
“BAFF Promotes Th17 Cells and Aggravates Experimental Autoimmune Encephalomyelitis”.
PloS One, 2011; 6(8): Published online 2011 August. doi: 10.1371, PMCID: PMC**
28. Yujiro Kida, Zan Xian Xia, Sujun Zheng, Nick M. Mordwinkin, Stan G. Louie, Song Guo Zheng, Min Feng, Hongbo Shi, Zhongping Duan, and Yuan-Ping Han*. “Interleukin-1 as an injury signal mobilizes retinylesters in hepatic stellate cells through down regulation of lecithin retinol acyltransferase”.
PLoS One, 2011. 6(11): e26644. doi:10.1371/journal.pone.**
29. Ling Lu, Jilin Ma, Zhiyuan Li, Qin Lan, Maogen Chen, Ya Liu, Zanxian Xia, Julie Wang, Yuan-Ping Han, Wei Shi, Valerie Quesniaux, Bernhard Ryffel, David Brand, Bin Li, Zhongmin Liu, Song Guo Zheng.
“All-Trans Retinoic Acid Promotes TGF-β-Induced Tregs via Histone Modification but Not DNA Demethylation on Foxp3 Gene Locus”.
PloS One, 2011; 6(9): e24590. doi:10.1371/journal.pone.**.
30. Liyan Chen, Feng Ren, Haiyan Zhang, Tao Wen, Zhengfu Piao, Li Zhou, Sujun Zheng, Jing Zhang, Yu Chen, Yuanping Han, Zhongping Duan, Yingji Ma.
“Inhibition of Glycogen Synthase Kinase 3b Ameliorates D-GalN/LPS-Induced Liver Injury by Reducing Endoplasmic Reticulum Stress-Triggered Apoptosis”
PLoS One, 2011. September 2012 | Volume 7 | Issue 9 | e45202
31. Yuan-Ping Han*, Ming Kong, Sujun Zheng, Yang Ren, Hongbo Shi, and Zhongping Duan.
“Vitamin D In Liver Diseases: From Mechanisms to Clinical Trials”.
Journal of Gastroenterology and Hepatology. 2013; 28, Suppl.1: 49–55
32. Ling Lu, Min Feng, Lan Qin et al., Yuan-Ping Han*.
“Restoration of intrahepatic regulatory T cells through MMP-9/13-dependent activation of TGF-β is critical for immune homeostasis following acute liver injury”.
Journal of Molecular Cell Biology. (2013) 5 (6): 369-379
33. Wei L, Ren F, Zhang X, Wen T, Shi H, Zheng S, Zhang J, Chen Y, Han Y, Duan Z.
“Oxidative stress promotes D-GalN/LPS-induced acute hepatotoxicity by increasing glycogen synthase kinase 3β activity”.
Inflammation Research. 2014 Jun; 63(6):485-94. doi: 10.1007/s00011-014-0720-x. Epub 2014 Feb 16.
34. Kong M, Zhu L, Bai L, Zhang X, Chen Y, Liu S, Zheng S, Pandol SJ, Han YP, Duan Z.
“Vitamin D deficiency promotes nonalcoholic steatohepatitis through impaired enterohepatic circulation in animal model”.
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