Cell Death: Mechanism and Disease PDF
Preview Cell Death: Mechanism and Disease
Hao Wu Editor Cell Death Mechanism and Disease Cell Death Hao Wu Editor Cell Death Mechanism and Disease Editor Hao Wu Department of Biological Chemistry and Molecular Pharmacology Harvard Medical School Boston , MA , USA Program in Cellular and Molecular Medicine, Boston Children’s Hospital Boston, MA, USA ISBN 978-1-4614-9301-3 ISBN 978-1-4614-9302-0 (eBook) DOI 10.1007/978-1-4614-9302-0 Springer New York Heidelberg Dordrecht London Library of Congress Control Number: 2013952922 © Springer Science+Business Media New York 2014 This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifi cally the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfi lms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. Exempted from this legal reservation are brief excerpts in connection with reviews or scholarly analysis or material supplied specifi cally for the purpose of being entered and executed on a computer system, for exclusive use by the purchaser of the work. Duplication of this publication or parts thereof is permitted only under the provisions of the Copyright Law of the Publisher’s location, in its current version, and permission for use must always be obtained from Springer. Permissions for use may be obtained through RightsLink at the Copyright Clearance Center. Violations are liable to prosecution under the respective Copyright Law. The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specifi c statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. While the advice and information in this book are believed to be true and accurate at the date of publication, neither the authors nor the editors nor the publisher can accept any legal responsibility for any errors or omissions that may be made. The publisher makes no warranty, express or implied, with respect to the material contained herein. Printed on acid-free paper Springer is part of Springer Science+Business Media (www.springer.com) Foreword The concept of “apoptosis” as a regulated cell death pathway in mammalian cells was fi rst proposed by Andrew Wyllie based on an intriguing observation made dur- ing his Ph.D. study that showed dying cancer cells having DNA fragmentation. While Wyllie’s work could had been easily dismissed as a “descriptive” study by today’s standard and rejected outright, it laid the foundation for the subsequent decades of studies that led to the understanding of the molecular mechanisms of apoptosis. Now the concept of cellular “suicide” is no longer a strange or a novel idea. It has been generally accepted that regulation of cell death is important for development as well as for the maintenance of the normal tissue homeostasis. The studies on apoptosis led to many conceptual advances that helped us to understand the disease mechanisms. The molecular mechanism that protects mam- malian cells from apoptosis were fi rst illustrated by the ground-breaking work from the group of David Vaux and colleagues who showed the ability of Bcl-2 when overexpressed to prolong the survival of cancer cells. Vaux’s work provided the second most important principle in oncogenesis, after the uncontrolled and exces- sive proliferation, that tumor cells must develop mechanisms to evade apoptosis. The two decades of research on Bcl-2 family provided the molecular understanding as how pro- and anti-apoptotic members of Bcl-2 family interact and control the cellular survival. This understanding provided the crucial insights as how such interactions may be manipulated pharmacologically. The exclusive dependence of cancer cell survival on the apoptosis inhibitory effect of Bcl-2 family is now being explored for therapeutic benefi ts in the treatment of cancers. The execution of apoptosis in mammalian cells is mediated by the evolution- arily conserved caspase family, a principle fi rst illustrated by the works from my own group. Mammalian caspase family is rather large with at least 12 members which is almost certain due to the complicated tasks that these caspases are involved in. These caspases are arranged into amplifi cation cascades that control either the “intrinsic apoptosis” pathway regulated by the mitochondrial pathway which leads to the activation of “apoptosome” or the “extrinsic apoptosis” path- way which is activated by the ligands of death receptor family. Caspases can be activated to mediate apoptosis by a wide range of physiological and pathological v vi Foreword signaling in different cell types: from DNA damage in cancer cells to tropic factor deprivation in neurons. The consequence of caspase activation, however, is not always lethal: in neurons, limited and localized caspase activation has now been implicated in modulating synaptic plasticity or mediating neurite pruning in fi ne tuning of neuronal circuitry. The two decades of research on cell death broke some of the historical dogma such as necrosis can only be passive cell death. It turns out that when apoptosis fails to occur, cells may undergo a form of regulated necrosis, termed “necroptosis” or “programmed necrosis.” Necroptosis activated by TNFα is the most understood necrotic cell death pathway. Stimulation of type I TNF receptor by TNFα leads to the transient formation of a membrane complex associated with the intracellular death domain of TNFR1, called “complex I” which includes adaptor protein TRADD, RIP1, and E3 ubiquitin ligases TRAF2 and cIAP1/2. The complex I is then transitioned into one of the two alternative intracellular signaling complexes, “complex IIa” or “complex IIb.” The complex IIa, which includes FADD, caspase-8, and RIP1, leads to the activation of caspase-8 and apoptosis. On the other hand, under certain conditions when apoptosis fails to be activated, an alternative complex that includes RIP1 and RIP3 kinases is formed. The kinase activity of RIP1 is required for the formation of complex IIb to mediate necroptosis and sometimes is also involved in mediating the activation of caspases with complex IIa in the absence of cIAP1/2. Interestingly, as shown by Hao Wu’s group, the complex IIb formed by RIP1 and RIP3 involves the formation of amyloid-like structure. Given the wide association of amyloid-like structures in neurodegenerative diseases, the formation of amyloid structure in a regulated necrotic cell death pathway is very intriguing. The involvement of RIP1 kinase in mediating acute neurological injuries has already been suggested by the ability of necrostatin-1, a highly specifi c inhibitor of RIP1 kinase, to protect a wide range of animal models induced by ischemia. It will be interesting to examine the involvement of RIP1–RIP3 amyloid complexes in human neurodegenerative diseases in future. The history of cell death research argues strongly for the important value of investigators initiated and curiosity-driven research. While there are certainly val- ues for “-omics” approaches where we may get to systematically understand the physical nature of our cells, our body, and our genetic compositions, the mecha- nisms that control cell death certainly would not had been understood without the hypothesis-driven researches as that had occurred. The researches on cell death mechanisms also provide an excellent example where excellence in basic scientifi c research not only led to molecular insights to our living world in general but also can be translated into medicines that can treat diseases to improve our lives. A cell that dies is never in vain. Boston , MA , USA Junying Yuan Pref ace As editor of this book, I wish to thank several important people, without whose assistance a successful outcome would not have been possible. I was originally approached by Dr. Portia E. Formento, an Editor of Springer Science + Business Media, during the Biophysical Society Meeting in Baltimore, Maryland, in March, 2011, about editing a book on cell death. I hesitated at fi rst. While scientists are always busy, it was an extra busy time for me as my son Alex was preparing to go to college and I was contemplating fresh job opportunities. Portia was convincing enough to persuade me that such a book would be both valuable and timely and that Springer would assist me in accomplishing this at my own pace. I am deeply indebted to her for her support and encouragement. Although I signed up for the job of putting such a book together then, I did not begin to contact potential contributors until more than a year later, a couple of months before my lab’s move from Weill Cornell Medical College to Boston Children’s Hospital and Harvard Medical School. Fortunately, the theme of the book, titled “Cell Death: Mechanism and Disease,” is exactly as intended and cov- ers the molecular basis of cell death—apoptotic and necrotic—as well as the rele- vance of cell death mechanisms to understanding, preventing, and treating human disease. I have had the pleasure of working in this highly exciting and competitive fi eld for the past 16 years and have seen its rapid evolution, with one surprising fi nd- ing after another. The book strives to present a balanced and comprehensive view of the current state of the art. I am particularly grateful to all the wonderful contributors who truly made the book possible. They are not only amazing scientists but also good friends whom I have come to know over the years. I am especially indebted to David Vaux, a pio- neering fi gure in cell death research, for his commitment to and enthusiasm about the book. Earlier this year, I had the honor of visiting “Davo” (short for Dave Vaux) and his family in Melbourne, where I experienced his hospitality fi rsthand. I would also like to praise my dear colleague and friend Junying Yuan for writing such a beautiful forward for the book. I am extraordinarily thankful to Daniel L. Dominguez, vii viii Preface the Developmental Editor of the book, who pushed and shoved and made sure that things got done on time. Finally, I take this opportunity to express my appreciation for the boundless love around me, my children Alex and Michael who are my joy and pride, and my current and former lab members who are the heroes behind every research accomplishment from my laboratory. It is my wish that you will enjoy reading the book as much as I have enjoyed edit- ing it, regardless of whether you are an amateur or an expert in the cell death fi eld. Boston , MA , USA Hao Wu Contents 1 Historical Perspective: The Seven Ages of Cell Death Research ........ 1 David L. Vaux 2 The Intrinsic Apoptotic Pathway ........................................................... 15 Xuejun Jiang 3 Molecular Basis of Cell Death Programs in Mature T Cell Homeostasis................................................................ 41 Carrie L. Lucas and Michael J. Lenardo 4 Bcl-2 Family and Their Therapeutic Potential ..................................... 61 Qian Liu, Xiaoke Chi, Brian Leber, and David W. Andrews 5 IAP Proteins and Their Therapeutic Potential .................................... 97 Domagoj Vucic 6 Cell Death and Cancer ............................................................................ 121 David L. Vaux 7 The DNA Damage Response Mediates Apoptosis and Tumor Suppression .......................................................................... 135 Katherine Baran, Diego Rodriguez, and Douglas Green 8 Neuronal Death Mechanisms in Development and Disease ................ 167 Corey L. Cusack, Ryan P. Annis, Adam J. Kole, and Mohanish Deshmukh 9 The Complex Interplay Between Metabolism and Apoptosis ............. 189 Kelly Lindblom and Sally Kornbluth 10 Programmed Necrosis/Necroptosis: An Infl ammatory Form of Cell Death ............................................................................................ 211 Francis Ka-Ming Chan ix
The list of books you might like
