中科大校友Science Signal凋亡细胞发挥“余热”

　　

生物通报道，科罗拉多州大学医学院放射性癌症学系，上海交通大学附属第一人民医院，上海交通大学癌症研究所，科罗拉多州大学医学院药理系的科学家在最近一期的Science Signal上发表文章Apoptotic Cells Activate the "Phoenix Rising" Pathway to Promote Wound Healing and Tissue Regeneration，解析凋亡细胞在组织修复过程中的积极作用。

 

文章通讯作者是来自科罗拉多州大学放射与癌症生物学中心的李传元教授（Chuan-Yuan Li，生物通译），其早毕业于中国科技大学，在哈佛大学获得博士学位，主要从事肿瘤、放射性肿瘤学等方面的研究。

 

其他参与研究的还有科罗拉多州大学的Fang Li、Jiang Chen、Yuanlin Peng，上海交通大学医学院的黄倩教授。

 

细胞凋亡，被誉为细胞“绝唱”，有趣的是，李传元教授等人发现，凋亡细胞在死亡阶段还能发挥“余热”，在组织修复和再生过程中发挥重要作用。损伤组织修复再生是多细胞生物共有的特征。

 

李传元等人发现，在组织中，凋亡细胞可以释放一种生长信号刺激祖细胞和干细胞增殖生长，促进组织损伤愈合。

 

在这个过程中，发挥关键作用的是caspase3与7，它们是两种活性蛋白酶，在西部凋亡程序过程中执行细胞死亡程序。研究小组以小鼠为模型，对caspase3与caspase7进行功能缺失研究，结果发现，缺失两种蛋白酶的小鼠皮肤和肝脏修复过程受阻。

 

在caspase3与caspase7的下游，发挥作用的是前列腺素E2（具有促进干细胞或祖细胞增殖，具有促进组织再生作用），研究者们将这一通路过程称为“phoenix rising”通路。

 

这一研究为了解组织修复与再生，进一步了解凋亡机制开辟了新的视野。

（生物通 张欢）

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生物通推荐原文检索

Apoptotic Cells Activate the "Phoenix Rising" Pathway to Promote Wound Healing and Tissue Regeneration

Fang Li1, Qian Huang1,2,3, Jiang Chen4,5, Yuanlin Peng6, Dennis R. Roop4,5, Joel S. Bedford6, and Chuan-Yuan Li1,5,7*

 

1 Department of Radiation Oncology, University of Colorado School of Medicine, Aurora, CO 80045, USA.

2 Center for Laboratory Research, First People’s Hospital, Shanghai Jiaotong University, Shanghai 200080, China.

3 National Laboratory for Oncogene and Related Genes Research, Cancer Institute of Shanghai Jiaotong University, Shanghai 200032, China.

4 Department of Dermatology, University of Colorado School of Medicine, Aurora, CO 80045, USA.

5 Charles C. Gates Regenerative Medicine and Stem Cell Biology Program, University of Colorado School of Medicine, Aurora, CO 80045, USA.

6 Department of Environmental and Radiological Health Sciences, Colorado State University, Fort Collins, CO 80523, USA.

7 Department of Pharmacology, University of Colorado School of Medicine, Aurora, CO 80045, USA.

 

【Abstract】

The ability to regenerate damaged tissues is a common characteristic of multicellular organisms. We report a role for apoptotic cell death in promoting wound healing and tissue regeneration in mice. Apoptotic cells released growth signals that stimulated the proliferation of progenitor or stem cells. Key players in this process were caspases 3 and 7, proteases activated during the execution phase of apoptosis that contribute to cell death. Mice lacking either of these caspases were deficient in skin wound healing and in liver regeneration. Prostaglandin E2, a promoter of stem or progenitor cell proliferation and tissue regeneration, acted downstream of the caspases. We propose to call the pathway by which executioner caspases in apoptotic cells promote wound healing and tissue regeneration in multicellular organisms the "phoenix rising" pathway.

 

Chuan-Yuan Li

Professor of Radiation Oncology/Pharmacology

University of Colorado Health Sciences Center

 

Education

B.S. in Chemistry, 1987, University of Science & Technology, Hefei, China.

Ph.D. in Cancer Biology, 1993, Harvard University, Cambridge, MA.

 

Professional Experience

2006-  Professor of Pharmacology, University of Colorado Health Sciences Center, Aurora,

CO.

2006-  Professor and Director, Division of Radiation and Cancer Biology, Dept. of

Radiation Oncology, University of Colorado Health Sciences Center, Denver, CO.

2005-2006  Professor, Departments of Radiation Oncology, Pharmacology and Cancer Biology

Duke University Medical Center, Durham, NC

2002-2005  Associate Professor, Dept. of Radiation Oncology, Duke University Medical Cente

Durham, NC 

1997-2002  Assistant Professor, Dept. of Radiation Oncology, Duke University Medical Cent

Durham, NC 

1993-1996  Postdoctoral research fellow, Harvard University, Boston, MA

 

Honors and Awards

1987-89  Rohm and Haas Fellowship for graduate study at Harvard University

1990  Student Travel Award, 39th Radiation  Research Society Annual Meeting, Ne

Orleans, LA

1991  Student Travel Award, 9th International Congress of Radiation Research, Toron

CA

1993    Kresge Center for Environmental Science pilot grant, Harvard University

1999    Komen Foundation Grant for Breast Cancer Research 

2001    Best Poster Award, Annual Meeting of the Duke University Cancer Center

2002  Best Proffered Paper, 6th

 Wolfsberg Symposium in Radiation Oncology, Ematingen,

Switzerland, 2002

2006  Michael Fry Research Award from the Radiation Research Society, Philadelphia,

PA.