{"id":2564,"date":"2015-09-17T00:00:00","date_gmt":"2015-09-17T07:00:00","guid":{"rendered":"https:\/\/vermont.salk.edu\/news-release\/not-all-organs-age-alike\/"},"modified":"2015-11-15T08:12:03","modified_gmt":"2015-11-15T16:12:03","slug":"not-all-organs-age-alike","status":"publish","type":"disclosure","link":"https:\/\/www.salk.edu\/de\/news-release\/not-all-organs-age-alike\/","title":{"rendered":"Not all organs age alike"},"content":{"rendered":"

\nLA JOLLA\u2013Aging is typically thought of as the gradual decline of the whole body, but new research shows that age affects organs in strikingly different ways. A study published September 17, 2015 in Cell Systems<\/a><\/em> provides the first comprehensive view of how cellular proteins age in different organs, revealing major differences between the liver and brain in young and old rats. The findings suggest that how an organ ages may depend on its unique cellular properties and its physiological function in the body.\n<\/p>\n

\n\u201cOur study showed that organs have different aging mechanisms and that aging is largely driven by changes in protein production and turnover,\u201d says co-senior author Martin Hetzer<\/a>, Salk professor and holder of the Jesse and Caryl Philips Foundation Chair.<\/p>\n

\n\u201cChanges that occur in aging can be diverse and difficult to pin down, and looking simply at one parameter might result in not seeing the whole picture,\u201d says co-first author Brandon Toyama, Salk research associate. However, harnessing the power of several state-of-the-art technologies has let the group see age-dependent changes that could not be seen before. The result, according to Toyama, is \u201ca rich resource that should stimulate the generation of new experimentally testable hypotheses, leading to a better understanding of aging on the organism level.\u201d<\/p>\n

\"\"<\/p>\n

Scientists provide the first comprehensive view of how cellular proteins age in different organs, revealing major differences between the liver and brain in young and old rats.<\/p>\n

Klicken Sie hier<\/a> f\u00fcr ein hochaufl\u00f6sendes Bild.<\/p>\n

\nBild: Mit freundlicher Genehmigung des Salk Institute for Biological Studies\n<\/p>\n<\/div>\n

\nAging causes the progressive deterioration in the function of organs, as well as the functions of cells and proteins within them. Past studies have shown that the activity level of genes also changes with age, with most genes showing similar changes in expression across organs. However, a recent large-scale study showed that the vast majority of proteins across different organs don\u2019t change in abundance during aging. These findings have left it unclear how aging affects cellular proteins and whether age-related changes that affect proteins differ across organs.<\/p>\n

\nTo answer these questions, Toyama and Hetzer, along with co-first author Alessandro Ori of the European Molecular Biology Laboratory<\/a> (EMBL), and senior authors Nicholas Ingolia of the University of California, Berkeley<\/a> and Martin Beck of EMBL took an integrated \u201comics\u201d approach instead of focusing on one isolated aspect of gene expression as in past studies. The combination of genomics and proteomics allowed them to simultaneously analyze changes in transcription, translation, protein levels, alternative splicing and protein phosphorylation to gain a comprehensive and quantitative view of protein differences in the liver and brain of young and old rats. <\/p>\n

\nThey identified 468 differences in protein abundance between young and old animals, mainly due to changes in protein synthesis. Another set of 130 proteins showed age-related changes in their location within cells, phosphorylation state, or splice form\u2013changes expected to affect the activity level or function of the proteins. \u201cOur work significantly expands the list of proteins that are affected by chronological age in mammals,\u201d Beck says. \u201cIn most cases, individual datasets would not have been sufficient to extrapolate these networks, highlighting the complexity of the effects of chronological age on the proteome and the benefits of our integrative approach.\u201d<\/p>\n

\nStrikingly, most of these age-related protein differences were specific to one organ. The protein aging patterns seem to relate to the organ\u2019s specific cellular properties or function. Because cells in the liver are frequently replaced throughout adulthood, this organ has ample opportunity to replenish its proteins. By contrast, most neurons in the adult brain are non-dividing cells that must survive for an organism\u2019s entire lifetime, so the longer-lived proteins in the brain are more vulnerable to the accumulation of damage and loss of function over time. <\/p>\n

\nAs a result, a larger fraction of proteins was affected by aging in the brain compared to the liver. In the brain, aging altered proteins involved in neuronal plasticity and memory formation, whereas several metabolic networks were altered in the liver. \u201cBased on our findings, we would define aging as an organ-specific deterioration of the cellular proteome,\u201d says Hetzer.<\/p>\n

\nIn future studies, the researchers will analyze other organs such as the heart to further examine the general and organ-specific effects of aging, and investigate how and why these changes occur. \u201cWe expect these organs to have specific aging signatures, like the brain and liver,\u201d Hetzer says. \u201cAn interesting open question is whether one organ can affect the aging of another organ, that is, is aging sensed at the organismal level? Answering this question would give us a more comprehensive understanding of the aging process and how it relates to disease.\u201d<\/p>\n

\nThe researchers will also study how aging differs across individuals to determine the role of genetic variability. \u201cThis research may shed new light on the molecular mechanisms underlying age-related diseases, enabling the identification of risk factors to predict which individuals are most susceptible based on their genetic makeup,\u201d Beck says. \u201cIn the end, a better understanding of the molecular mechanisms of aging could lead to the development of novel therapies to prevent or treat a range of age-related diseases.\u201d<\/p>\n

\nThis research was supported by the European Molecular Biology Laboratory, the Alexander von Humboldt Foundation<\/a>, der Marie Sk\u0142odowska-Curie Actions<\/a>, der Searle Scholars Program<\/a> und die Paul F. Glenn Center for Aging Research<\/a>. <\/p>\n

Content courtesy of Cell Press<\/a>.<\/p>\n

About Cell Systems:<\/strong>
\nCell Systems<\/em>, published by Cell Press, is a new monthly journal featuring papers that provide, support, or apply systems-level understanding in the life sciences and related disciplines. Research describes novel discoveries, milestone achievements, applied research, translational findings, broadly useful tools or resources, or insights into the use of technology. For more information, please visit http:\/\/www.cell.com\/cell-systems<\/a>. To receive media alerts for Cell Systems or other Cell Press journals, contact press@cell.com<\/a>. <\/p>\n

\nAbout EMBL:<\/strong>
\nEMBL is Europe\u2019s flagship laboratory for the life sciences, with more than 80 independent groups covering the spectrum of molecular biology. EMBL is international, innovative and interdisciplinary\u2014its 1,600 employees, from many nations, operate across five sites: the main laboratory in Heidelberg, and outstations in Grenoble; Hamburg; Hinxton, near Cambridge (the European Bioinformatics Institute); and Monterotondo, near Rome. Founded in 1974, EMBL is an inter-governmental organisation funded by public research monies from its member states. The cornerstones of EMBL\u2019s mission are: to perform basic research in molecular biology; to train scientists, students and visitors at all levels; to offer vital services to scientists in the member states; to develop new instruments and methods in the life sciences and actively engage in technology transfer activities, and to integrate European life science research. Around 230 students are enrolled in EMBL\u2019s International PhD programme. Additionally, the Laboratory offers a platform for dialogue with the general public through various science communication activities such as lecture series, visitor programmes and the dissemination of scientific achievements.<\/p>","protected":false},"featured_media":0,"template":"","faculty":[86],"disease-research":[],"class_list":["post-2564","disclosure","type-disclosure","status-publish","hentry","faculty-martin-hetzer"],"acf":[],"yoast_head":"\nNot all organs age alike - Salk Institute for Biological Studies<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/www.salk.edu\/de\/news-release\/not-all-organs-age-alike\/\" \/>\n<meta property=\"og:locale\" content=\"de_DE\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Not all organs age alike - Salk Institute for Biological Studies\" \/>\n<meta property=\"og:description\" content=\"LA JOLLA\u2013Aging is typically thought of as the gradual decline of the whole body, but new research shows that age affects organs in strikingly different ways. 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