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Montagna Symposium 2014—Skin Aging: Molecular Mechanisms and Tissue Consequences Barbara A View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector MEETING REPORT Montagna Symposium 2014—Skin Aging: Molecular Mechanisms and Tissue Consequences Barbara A. Gilchrest1, Judith Campisi2, Howard Y. Chang3,GaryJ.Fisher4 and Molly F. Kulesz-Martin5 Journal of Investigative Dermatology (2015) 135, 950–953; doi:10.1038/jid.2014.546 The 63rd annual Montagna Symposium theory proved extremely difficult to test that are regulated by NF-kB, focusing on on the Biology of Skin, ‘‘Skin Aging: because mutations and epimutations Lethe, which is induced by NF-kBand Molecular Mechanisms and Tissue Con- occur at low frequency, turning each in turn dampens the NF-kBresponse, sequences,’’ was held from 9–13 Octo- tissue into genome mosaics. Dr Vijg helping cells forget that they were ber 2014, in Gleneden Beach, Oregon. presented data from his group on their stressed in the past. Chang concluded The meeting brought together basic single-cell approach to the study of by describing a new technology that can gerontologists, dermatologists, and skin somatic DNA mutations and epimuta- map chromatin changes in just a few biologists working on mechanisms and tions in aging tissues. Making use of the thousand cells, finding that many age- problems of skin aging, industry scien- most recent next-generation sequencing associated changes are only evident in tists attempting to create products to methods, their data indicated that the the long-lived stem cell compartment of address unmet needs in the field, and frequency of somatic mutations is much tissue. trainees wishing to acquire a better higher than previously thought, with Ruby Ghadially discussed functional understanding of the aging process and many mutations inactivating gene func- studies of human epithelial stem cells. its consequences in the skin. The many tion. Dr Vijg discussed these results in Although human skin stem cells can be recent advances in both basic and the context of some broader philosophi- enriched by one or more cell surface applied aspects of cutaneous aging led cal and ethical questions posed by the markers, their functional characteriza- to productive exchanges among these study of aging. For example, in view of a tion had previously depended on participants, broadened everyone’s hor- gradual erosion of genome and epigen- in vitro colony-forming assays. Dr Gha- izons, and stimulated several new col- ome integrity, is it feasible to develop dially showed that intradermal injection laborations. The Symposium was interventions to delay, halt, or even of skin stem cells can recapitulate some chaired by Barbara A. Gilchrest with revert aging, and are there ethical costs? aspects of wound healing and lead to Session Chairs Judith Campisi, Howard This discussion provided participants the formation of epidermal inclusion Chang, and Gary Fisher. with an engaging, big-picture introduc- cysts where cells undergo keratiniza- The meeting opened with a Keynote tion to the meeting’s theme. tion. This assay system also allowed presentation by Jan Vijg. Dr Vijg began Session Chair Howard Chang drew comparison of the proliferative capacity by pointing out the great progress that the connection between aging and stu- of epithelial stem cells in vivo, albeit in has been made over the last two cen- dies of epigenetics—the mechanisms of a xenograft setting, and can be used to turies in increasing both life expectancy gene memory over time—and then compare stem cells in different settings, and health span––i.e., the average time introduced recent findings that the including aging. span an individual can expect to remain human genome encodes thousands of If seeing is believing, Valentina Greco functional. However, further progress long noncoding RNAs, many of which continued the session with an exciting depends entirely on gaining a deeper have functions in chromatin regulation. presentation on in vivo imaging of stem understanding of the intrinsic mechan- Chang reported that the stress-respon- cell niche. Dr Greco developed cutting- isms that underlie the aging process and sive transcription factor NF-kBis edge two-photon microscopy methods predisposition to disease. Among the increasingly active with age in the skin and transgenic animals with fluorescent many theories of how we age, one of and other tissues and that interruption of nuclei in skin cells in order to make the oldest is based on the accumulation NF-kB activity in aged skin can restore movies of how individual cells in of errors in genome and epigenome. many features of young skin. He hair follicles move and develop. Although conceptually fairly simple, this then described long noncoding RNAs Direct visualization of cell dynamics 1Dermatology Service, Massachusetts General Hospital, Boston, Massachusetts, USA; 2Buck Institute for Research on Aging, and Lawrence Berkeley National Laboratory, Novato, California, USA; 3Department of Dermatology, Stanford University, Stanford, California, USA; 4Department of Dermatology, University of Michigan, Ann Arbor, Michigan, USA and 5Department of Dermatology, Oregon Health & Science University, Portland, Oregon, USA Correspondence: Molly F. Kulesz-Martin, Department of Dermatology, Oregon Health & Science University, L468R, 3181 SW Sam Jackson Park Road, Portland, Oregon 97239, USA. E-mail: [email protected] 950 Journal of Investigative Dermatology (2015), Volume 135 & 2015 The Society for Investigative Dermatology BA Gilchrest et al. Montagna Symposium 2014: Skin Aging overturned several dogmas in the skin pharmacologic alleviation of endoplas- sequences de novo. Long-term exposure stem cell field, including the idea that mic reticulum stress. to T-oligos mimics the effects of short, stem cells are somehow uniquely speci- Session Chair Judith Campisi intro- dysfunctional telomeres, but short-term fied. In fact, if existing hair follicle stem duced the multifaceted stress response exposure to T-oligos elevates DNA cells are destroyed, other cells can take termed cellular senescence. Senescent repair capacity, increases telomerase their place, influenced by the unique cells are characterized by an essentially activity, and elongates telomeres. These environment of the niche. During hair irreversible arrest of cell proliferation studies indicate another doubled-edged follicle regression in catagen, Dr Greco and a complex senescence-associated sword. At low levels, DNA damage showed that only the outer root sheath secretory phenotype composed of signaling, such as that caused by short- cells die, whereas the inner root sheath numerous growth factors, inflammatory term T-oligo exposure, is protective, cells move up the follicle. The signal for cytokines, and proteases. The senes- increasing DNA repair systems, telomer- outer root sheath cells to die emanates cence growth arrest is known to be an ase expression, and telomere length. At from mesenchymal cells in the dermal important tumor suppressive mechan- higher levels, such as that caused by papilla. These results raised the concept ism. The senescence-associated secre- long-term T-oligo and excessive sun that the mesenchymal cells in the der- tory phenotype, however, is a double- exposures, the protective effects are over- mal papilla may be the intrinsic clock edged sword. Using a mouse model that whelmed and DNA damage signaling for hair follicle cycling over time. allows the visualization, sorting, and then drives apoptosis and senescence. Ray Monnat followed with studies of selective elimination of senescent cells, Steven Artandi closed the session by the Werner Syndrome, a disease with Campisi presented evidence that skin elucidating how telomerase expression many features of premature aging aris- wounding is accompanied by a rapid and assembly are controlled. In both ing from loss of function mutations in but transient appearance of senescent mice and humans, the identification the WRN helicase gene. A consequence cells, primarily fibroblasts and endothe- of telomerase-positive cells has been of this progeroid syndrome is the lial cells that secreted platelet-derived elusive owing to the very low expression increased incidence of cancers, includ- growth factor AA, a newly identified of the holoenzyme components. The ing melanoma, with an over 50-fold senescence-associated secretory pheno- Artandi laboratory recently overcame increase in Werner Syndrome patients. type factor that was essential for optimal this limitation by generating a knock-in Dr Monnat identified several aspects of wound closure. By contrast, the chronic reporter mouse model in which the DNA metabolism that are altered in presence of senescent cells, which can open reading frame of TERT, the reverse Werner Syndrome cells. He found that occur in response to whole-body radia- transcriptase subunit of the enzyme, is the rate of the DNA replication fork tion, systemic genotoxic chemotherapy, replaced by fluorescent proteins, allow- progression is altered, and many genes or oxidative stress, is deleterious and ing tracking of telomerase-positive stem exhibit altered expression levels. The can promote tumor metastasis and and transit amplifying cells and deter- changes in gene expression apparently retard skin wound healing. mining their role in telomere length had large effects on genes encoding Anne Chang followed with a presen- maintenance. New evidence suggests tRNA synthetase pathways; thus, unex- tation on the marked individual varia- that telomerase is assembled in sub- pectedly, a defect in DNA metabolism
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