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Apoptosis: a Role in Skin Aging?

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Apoptosis: a Role in Skin Aging? Apoptosis: A Role in Skin Aging? Anne R. Haake, Inna Roublevskaia, and Molly Cooklis Department of Dennatology, University of Rochester School of Medicine & Dentistry, Rochester, New York, U.S.A. Prevailing theories view aging as an outcome of both homeostasis as a feature of normal keratinocyte differenti­ programmed and stochastic events that occur over the ation and as a cellular endpoint of stress. To probe the lifetime of the individual. In this context, aging can be question of whether apoptosis contributes to the process defined as a progressive decline in homeostasis and a of skinaging, we present evidence for apoptotic dysregul­ period characterized by the inability of the organism to ation during aging in nonskin systems and discuss some respond adaptively to stress. Apoptosis thus stands out findings suggesting that decreased efficiency of apoptosis as a potential key cellular process that may be affected may contribute to the alterations characteristic of intrinsic during aging because apoptosis is both an important (chronologie) aging and extrinsic (photo aging) skin homeostatic mechanism and a protective cellular aging. Key words: elongationfactor 1-alphalsenescence.Journal response to stress. In this paper we introduce the topic of Investigative Dermatology Symposium Proceedings 3:28- of apoptosis, its regulation, and its roles in epidermal 35, 1998 s apoptosis a contributing mechanism of skin aging? To date, apoptosis, and its regulation, allows us to generalize much of what is with the exception of the process of neoplastic transformation, known in these organisms to mammalian cells, and also provides us there is very litde direct evidence on which to base evaluation with the tools to search for genetic homologies. The agents and events I of this question. It is informative, however, to consider the (growth factors, hormones, cytokines, UV and gamma irradiation, features and regulation of the apoptotic process, and the specific disruption in oxidative pathways, and cell matrix interactions) that can roles of apoptosis in the skin. Some insights may also be gained by activate thea poptoticp athway (reviewed in McConkey and Orrenhius, drawing parallels between mechanisms that control apoptosis and 1994; Kroemer et ai, 1995) are many and varied, yet, the pattern of mechanisms that are dysregulated in aged skin. apoptosis itself is highly conserved. This has led researchers in the field to hypothesize that there must be a limited number of shared effector C APOPTOSIS: DEFINITION, INCIDEN E, AND FUNCTIONS mechanisms that trigger a cornmon apoptotic pathway (Vaux and n Strasser, 1996; Kroemer et ai, 1995, 1997; Wyllie, 1995), an that Apoptosis is an evolutionarily co served, gene-directed, active cell idea M the h e n death that follows an orderly pattern of morphologic and biochemical has held true. oreover, identification and c aract rizatio of changes. Cornmon histologic observations have established that a strict individual events and regulatory points along the apoptotic pathway experimental systems (Wyllie, 1995; Kroemer et ai, 1997), sequence of events is shared by all apoptotic cells. These include loss in these have allowed the development of concep divide the of cell oc ntact accompanied by cell rounding and a smoothing of the tual models that cell surface, loss of cytoskeletal integrity, cell shrinkage with resultant pathway into three mechanistically distinctphases; induction, effector, and degradation [see Haake and Polakowska (1997) for review compaction of the cytoplasm and organelles, nuclear and chromatin a in condensation, chromatin fragmentation, formation of apoptotic bodies, the context of epidermal differentiation] . been and engulfinent. Throughout the various tissues of the organism The induction phase also has referred to as the initiation or apoptosis normally functions in developmental remodeling, regulation signaling phase (Kroemer et aI, 1995). Although the ultimate trigger of apoptosis has not been established, many proximate inducing of cell numbers, and defense against damaged, virus-infected, auto­ o reactive, and transformed cells (Kerr et ai, 1992; McConkey and conditions (see ab ve) have been identified. In the induction phase, these heterogeneous stimuli activate receptor- and nonreceptor-medi­ Orrenius, 1994; Polakowska et ai, 1994). ated signal transduction pathways and second messengers such as cAMP, REGULATION OF APOPTOSIS: PRIVATE AND PUBLIC inositol triphosphate, diacylglycerol, and cerarnides (McConkey and PATHWAYS Orrenius, 1994; Hunan and Obeig, 1995). The pathways are not reserved for apoptotic signaling but also are used for other cellular The fact that apoptosis is gene-directed has spurred an enormous functions, such as growth control. The outcome of signaling depends number of studies because of the obvious biologic and medical on the particular inducing stimulus (which may affect one or more significance of a form of cell death that can be modulated. Much of signal transduction pathways), the developmental or physiologic state what we understand today about control of apoptosis comes from of the cell, and the cell's lineage. Thus, a given stimulus may elicit a studies of invertebrate systems with powerful genetics such as the cell type-specific response. For these reasons the signaling pathways of nematode Caenorhabdhitis elegans Drosophila melanogaster. and the fruitfiy, the induction phase have been referred to as the "private" pathways Fortuitously, broad evolutionary conservation of the mechanism of (Kroemer et ai, 1997). A common outcome of the different signal transduction pathways that impacts on apoptosis is interference with the cell cycle. A major control of apoptotic susceptibility is determined cell Reprint requests to: Dr. Anne R. Haake, Box 697, Department of Dermato­ by the cycle and it's checkpoints (King and Cidlowski, 1995) that o logy, University of Rochester School of Medicine & Dentistry, 601 Elmwood prevent aberrant DNA synthesis and mitosis. It is f relevance for this Avenue, Rochester, NY 14642. discussion that many of the major cell cycle regulatory genes that have 1087-0024/98/$10.50· Copyright © 1998 by The Society for Investigative Dennatology, Inc. 28 VOL. 3, NO.1, AUGUST 1998 SKIN AGING AND APOPTOSIS 29 been identified as important in the control of apoptosis, also have of total cell numbers. Elegant studies of cell kinetics in the amphibian been implicated in the aging process. Some examples are the tumor epidermis (Budtz and Spies, 1987) have established that apoptosis is a suppressors p53 and Rb, and the c-fos proto-oncogene. Although controlling factor of the cell birth to cell death ratio. New cells are apoptosis can be induced from any phase of the cell cycle (Bertrand produced in the proliferative compartment, primarily the basal cell et aI, 1994), entry into the cell death pathway usually occurs with re­ layer, and are balanced by cell death (terminaldiff erentiation/apoptosis). entry of noncycling cells into the cycle or entry onto a defective cell In the toad more cells are produced than are needed to replace cycle (Colombel et ai, 1992). There is some evidence that entry into terminally differentiated keratinocytes that are lost by desquamation. apoptosis may require at least partial cycling (pandey and Wang, 1995), As a balancing mechanism, a significant number of cells become providing a possible mechanistic explanation of the failure of senescent apoptotic without completing differentiation. In human skin it is not cells to undergo apoptosis (Wang, 1995). so clear that excessive keratinocytes are normally produced in the The evolutionarily conserved effector pathway, common to all cell basal cell layer. The majority of cells therefore complete terminal types, is regulated by distinct classes of "cell death genes." For example, differentiation, which itself may be an elaborated apoptotic pathway genes of the bcl-2 family (Cory, 1995) can suppress cell death at the (Fesus et aI, 1991; Haake and Polakowska, 1993; Polakowska and transition from induction to effector phases. Many viral proteins such Haake, 1994). If thea poptotic pathway is the foundation ofkeratinocyte as human papilloma virus (HPV) E6 and E7, SV40 T, and adenovirus terminal differentiation, it follows that apoptosis must be completed E1 A, also inhibit cellular proteins controlling the induction phase of for normal epidermal function. Moreover, as suggested by Raff (1992) apoptosis and are effective in cell immortalization. Some genes are for all cell types, there is some evidence in the epidermis that apoptosis essential for cell death and appear to function in the common effector is the default pathway taken when homeostatic regulation goes awry. phase. In C. elegans, these genes are CED-3 and CED-4. CED-3 has One would predict then that premature apoptotic cells may be found homology with the mammalian interleukin 1-� converting enzyme in the spinous and basal celll ayers, in cases of homeostatic dysregulation (ICE), a cysteine protease belonging to the caspase family (Nicholson or after environmental insult, or that failure to complete apoptosis and Thornberry, 1997) . Recently, a mammalian homolog of CED-4, would result in retention of nuclei beyond the granular layer. Indeed, known as Apoptosis activating factor-1 (Apaf-1), has been discovered premature, excessive, or deficient apoptosis all have been linked to (Zou et ai, 1997). Apaf-1 is a novel 130 kDa protein isolated from homeostatic dysregulation characteristic of skin disorders. For example,
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