Special Issue "Apoptosis"
A special issue of Cells (ISSN 2073-4409).
Deadline for manuscript submissions: closed (31 January 2013)
Dr. Vladimir V. Didenko
Departments of Neurosurgery and Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030, USA
Phone: +713 794 7572
Fax: +713 794 7095
Interests: neural cell injury and programmed cell death; mechanisms of age-related neural cell death; methods to detect and control programmed cell death in vivo; development and application of nucleic acid-based nanoprobes and molecular machines
Cellular suicide is a fundamental property of animal cells from worms to humans and is essential for the life of an organism. Every second at least one million cells die by apoptosis in the human body. These deaths play roles in a multitude of processes including embryogenesis, development, defense against cancer and infections, self-tolerance in the immune system, etc.
Since the inception of the term in 1972 by Kerr, Wyllie, and Currie, the field of apoptosis has witnessed an outburst of findings and had several paradigm shifts. Studies have revealed the origins of apoptotic machinery going back over a billion years and have uncovered a variety of ways which cells have developed to activate and suppress the apoptotic program.
As the field expanded further, the very concept of apoptotic cell elimination changed. Today apoptosis is no longer viewed as an individual cellular event, but includes the externally-controlled elimination of apoptotic cells by phagocytes in the waste-management phase. At present apoptosis enjoys a celebrity status in cell biology. As the number of publications in the field skyrockets, it is essential to maintain high visibility of individual research. This is the compelling advantage of Open Access journals, such as Cells. This special issue of Cells is dedicated to Apoptosis. We welcome contributions about its mechanisms, role in normal and pathological processes and new techniques for its detection and analysis. Reviews as well as original papers are invited.
Dr. Vladimir V. Didenko
Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are refereed through a peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed Open Access quarterly journal published by MDPI.
Please visit the Instructions for Authors page before submitting a manuscript. For the first couple of issues the Article Processing Charge (APC) will be waived for well-prepared manuscripts. English correction and/or formatting fees of 250 CHF (Swiss Francs) will be charged in certain cases for those articles accepted for publication that require extensive additional formatting and/or English corrections.
- programmed cell death
- cytochrome c
- death receptors
- mitochondria-mediated pathway
- DNA damage
- apoptotic cell clearance
- apoptotic nucleases
Cells 2012, 1(4), 1133-1155; doi:10.3390/cells1041133
Received: 29 October 2012; in revised form: 15 November 2012 / Accepted: 21 November 2012 / Published: 23 November 2012| Download PDF Full-text (1163 KB)
Article: Apoptotic Volume Decrease (AVD) Is Independent of Mitochondrial Dysfunction and Initiator Caspase Activation
Cells 2012, 1(4), 1156-1167; doi:10.3390/cells1041156
Received: 14 November 2012; in revised form: 24 November 2012 / Accepted: 27 November 2012 / Published: 5 December 2012| Download PDF Full-text (364 KB) | Download XML Full-text
Cells 2013, 2(1), 124-135; doi:10.3390/cells2010124
Received: 24 January 2013; in revised form: 15 February 2013 / Accepted: 26 February 2013 / Published: 4 March 2013| Download PDF Full-text (192 KB) | Download XML Full-text
Review: Induction of Cell Death Mechanisms and Apoptosis by Nanosecond Pulsed Electric Fields (nsPEFs)
Cells 2013, 2(1), 136-162; doi:10.3390/cells2010136
Received: 24 December 2012; in revised form: 5 February 2013 / Accepted: 21 February 2013 / Published: 6 March 2013| Download PDF Full-text (808 KB) | Download XML Full-text
Cells 2013, 2(1), 163-187; doi:10.3390/cells2010163
Received: 5 February 2013; in revised form: 4 March 2013 / Accepted: 5 March 2013 / Published: 14 March 2013| Download PDF Full-text (190 KB) | Download XML Full-text
Cells 2013, 2(2), 202-223; doi:10.3390/cells2020202
Received: 4 February 2013; in revised form: 5 March 2013 / Accepted: 12 March 2013 / Published: 26 March 2013| Download PDF Full-text (523 KB) | Download XML Full-text
Cells 2013, 2(2), 266-283; doi:10.3390/cells2020266
Received: 14 February 2013; in revised form: 3 April 2013 / Accepted: 5 April 2013 / Published: 26 April 2013| Download PDF Full-text (322 KB) | Download XML Full-text
Cells 2013, 2(2), 294-305; doi:10.3390/cells2020294
Received: 31 January 2013; in revised form: 24 March 2013 / Accepted: 19 April 2013 / Published: 8 May 2013| Download PDF Full-text (637 KB) | Download XML Full-text
Cells 2013, 2(2), 330-348; doi:10.3390/cells2020330 (doi registration under processing)
Received: 15 April 2013; in revised form: 25 April 2013 / Accepted: 14 May 2013 / Published: 22 May 2013| Download PDF Full-text (293 KB) | Download XML Full-text
The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.
Type of Paper: Review
Title: The Anti-apoptotic Role of Neuroglobin
Author: Tom Brittain
Affiliations: School of Biological Sciences and Centre for Brain Research, University of Auckland, Auckland, New Zealand; E-Mail: T. Brittain@auckland.ac.nz
Abstract: The small heme-protein neuroglobin is expressed at high concentrations in certain brain neurons and in the rod cells of the retina. This paper reviews the many studies which have recently identified a protective role for neuroglobin, in a wide range of situations involving apoptotic cell death. The origins of this protective mechanism are discussed in terms of both experimental results and computational modeling of the intrinsic pathway of apoptosis, which show that neuroglobin can intervene in this process by reaction with released mitochondrial cytochrome c. An integrated model, based on the various molecular actions of both neuroglobin and cytochrome c, is developed, which accounts for the cellular distribution of neuroglobin.
Type of Paper: Review
Title: Regulation of Neutrophil Apoptosis
Authors: Takayuki Kato and Seiichi Kitagawa
Affiliation: Department of Physiology, Osaka City University, Graduate School of Medicine, Osaka, Japan; E-Mail: email@example.com
Abstract: Neutrophils are terminally differentiated cells, and undergo spontaneous apoptosis. Spontaneous neutrophil apoptosis is delayed or accelerated in the presence of various cytokines or chemical mediators, including granulocyte colony-stimulating factor (G-CSF), granulocyte-macrophage CSF (GM-CSF), tumor necrosis factor-a, and interferon-a and g. Modulation of neutrophil apoptosis by cytokines or chemical mediators produced at the inflammatory sites may be closely associated with the outcome of inflammation. Understanding of the molecular mechanisms regulating neutrophil apoptosis is important to develop new therapeutics for acute and chronic inflammatory disorders. In this review, we discuss the molecular mechanisms underlying neutrophil apoptosis.
Type of Paper: Review
Title: Glucocorticoid-Induced Apoptosis: Cellular and Tissue Effects and Clinical Implications
Authors: Amanda L. Gruver-Yates and John A. Cidlowski
Affiliation: Laboratory of Signal Transduction, National Institutes of Environmental Health Sciences, 111 T. W. Alexander Drive, Research Triangle Park, North Carolina 27709, USA; E-Mail: firstname.lastname@example.org
Abstract: Glucocorticoids are potent inducers of apoptosis in many cell types and tissues. Widely known for their metabolic and immunosuppressive effects, glucocorticoids are widely prescribed in clinical settings. This review will focus on the known mechanisms of glucocorticoid-induced apoptosis and outline what is known about the apoptotic response in cells and tissues of the body after exposure to glucocorticoids. Glucocorticoid-induced apoptosis is known to affect the skeletal system, muscular system, circulatory system, nervous system, endocrine system, reproductive system, and the immune system. Furthermore, there are many anti-apoptotic effects of glucocorticoids in certain cell types, such as cardiomyocytes and mammary epithelial cells. Lastly, this review will focus on the pro- and anti-apoptotic mechanisms induced by glucocorticoids in cancer and their clinical implications.
Type of Paper: Review
Title: The Regulatory Effects of Gap Junction Channels, Hemichannels and Connexins on Cell Apoptosis and Their Potential Pharmaceutical Control
Authors: Jérome Gilleron, Diane Carette, Dominique Segretain and Georges Pointis
Affiliation: INSERM U 1065, Centre Méditerranéen de Médecine Moléculaire, Nice, F-06204 Cedex 3, France; University of Nice Sophia Antipolis, 151 route Saint-Antoine de Ginestière BP 2 3194 06204 Nice Cedex 3, France; E-Mail: email@example.com
Abstract: Gap junction protein*connexins (Cxs) play essential roles in cell homeostasis, growth, differentiation and death. Cxs control cell apoptosis by different molecular mechanisms. First, gap junction channels and hemichannels facilitate the flux of apoptotic signals respectively between adjacent cells and between the extracellular and intracellular environments dependently of the cell types and the Cxs isoforms. Second, Cxs by themselves, independently from their functional role through channels or hemichannels, may act as signaling effectors capable of interacting with caspase in order to activate the canonical mitochondrial apoptotic pathway. In the present review, we will dissect these different Cx functions during apoptosis, providing future strategies for apoptosis-mediated cancer therapy.
Type of Paper: Review
Title: The Anti-apoptotic Role of Neurotensin
Authors: Christelle Devader, Sophie Béraud-Dufour, Thierry Coppola and Jean Mazella
Affiliation: Institut de Pharmacologie Moléculaire et Cellulaire, CNRS UMR 7275, Université de Nice-Sophia Antipolis, 660 route des Lucioles, 06560 Valbonne, France; E-Mail: firstname.lastname@example.org
Abstract: The neuropeptide neurotensin exerts numerous biological functions including an efficient anti-apoptotic role both in the central nervous system and in the periphery. This review summarizes studies which clearly evidenced the protective effect of neurotensin through its three known receptors. The pivotal involvement of the neurotensin receptor-3, also called sortilin, in the molecular mechanisms of the anti-apoptotic action of neurotensin has been analysed in neuronal cell death, in cancer cell growth and in pancreatic beta cells protection. The relationships between the anti-apoptotic role of neurotensin and important physiological and pathological contexts is discussed in this review.
Type of Paper: Review
Title: Morphological Features of Organelles During Apoptosis: An Overview
Authors: Maria Grazia Bottone 1,2, Giada Santin 1,2, Francesca Aredia 2, Graziella Bernocchi 1, Carlo Pellicciari 1 and Anna Ivana Scovassi 2
Affiliations: 1 Dipartimento di Biologia e Biotecnologie “L. Spallanzani”, Laboratorio di Biologia Cellulare e Neurobiologia, Università di Pavia, Italy; E-Mails: email@example.com (M.G.B.); giadasantin@ gmail.com (G.S.); firstname.lastname@example.org (G.B.); email@example.com (C.P.)
2 Istituto di Genetica Molecolare CNR, Pavia, Italy; E-Mails: firstname.lastname@example.org (F.A.); email@example.com (A.I.S.)
Abstract: The apoptotic programme leading to controlled cell dismantling implicates some perturbations of nuclear dynamics, as well as changes affecting organelle distribution. In human cells driven to apoptosis by different stimuli, we have recently investigated the morphological properties of several organelles, including mitochondria, lysosomes, endoplasmic reticulum and Golgi apparatus. In this review, we will discuss the body of evidence suggesting that organelles are generally relocated and/or degraded during apoptosis, and that different pro-apoptotic conditions could selectively affect specific organelles.
Type of Paper: Article
Title: Apoptotic Volume Decrease (AVD) is Independent of The Mitochondrial Pathway and Initiator Caspases
Authors: Emi Maeno 1, Takeshi Tsubata 2 and Yasunobu Okada 1
Affiliations: 1 Department of Cell Physiology, National Institute for Physiological Sciences, Okazaki 444-8585, Japan; E-Mail: firstname.lastname@example.org
2 Laboratory of Immunology, Tokyo Medical and Dental University Graduate School of Biomedical Science, Tokyo 113-8510, Japan
Abstract: Persistent cell shrinkage is a major hallmark of apoptotic cell death. The early-phase shrinkage, which starts within 30-60 min after apoptotic stimulation and is called apoptotic volume decrease (AVD), is known to be accomplished by activation of K+ channels and volume-sensitive outwardly rectifying (VSOR) Cl− channels in a manner independent of caspase-3 activation. However, it is controversial whether AVD depends on the mitochondrial pathway and activation of initiator caspases. Here, we observed that AVD is induced not only by a mitochondrial apoptosis inducer, staurosporine (STS), in WEHI-231 cells but also by a receptor-mediated apoptosis inducer, Fas ligand (FasL), in SKW6.4 cells which undergo Fas-mediated apoptosis without involvement of mitochondria. Overexpression of Bcl-2 failed to inhibit the STS-induced AVD in WEHI-231 cells. In HeLa cells stimulated with FasL or STS, the AVD induction was found to precede activation of caspase-8 and -9 and be resistant to pan-caspase blockers. Thus, it is concluded that the AVD induction is an upstream event of the mitochondrial apoptotic signaling pathway and initiator caspase activation.
Last update: 26 September 2012