{"id":14586,"date":"2017-08-30T00:00:27","date_gmt":"2017-08-30T07:00:27","guid":{"rendered":"https:\/\/vermont.salk.edu\/?post_type=disclosure&#038;p=14586"},"modified":"2024-01-30T15:30:09","modified_gmt":"2024-01-30T23:30:09","slug":"protein-turnover-clue-living-longer","status":"publish","type":"disclosure","link":"https:\/\/www.salk.edu\/zh\/news-release\/protein-turnover-clue-living-longer\/","title":{"rendered":"Protein turnover could be clue to living longer"},"content":{"rendered":"<p>LA JOLLA\u2014It may seem paradoxical, but studying what goes wrong in rare diseases can provide useful insights into normal health. Researchers probing the premature aging disorder Hutchinson-Gilford progeria have uncovered an errant protein process in the disease that could help healthy people as well as progeria sufferers live longer.<\/p>\n<div class=\"row\" style=\"\"><div class=\"col-md-12 col-md-push-0\"><div class=\"video-anchor\" id=\"video-mw4meDYZKqU\"><\/div><div class=\"embed-responsive embed-responsive-16by9\"> <iframe class=\"embed-responsive-item\" src=\"\/\/www.youtube.com\/embed\/mw4meDYZKqU?rel=0\" webkitallowfullscreen mozallowfullscreen allowfullscreen><\/iframe><\/div><!-- .embed-responsive --><\/div><!-- .col-md-*size --><\/div><!-- .\/row -->\n<p>Scientists at the Salk Institute found that protein synthesis is overactive in people with progeria. The work, described in <a href=\"https:\/\/www.nature.com\/articles\/s41467-017-00322-z\"><em>Nature Communications<\/em><\/a> on August 30, 2017, adds to a growing body of evidence that reducing protein synthesis can extend lifespan\u2014and thus may offer a useful therapeutic target to counter both premature and normal aging.<\/p>\n<p>&#8220;The production of proteins is an extremely energy-intensive process for cells,&#8221; says <a href=\"https:\/\/www.salk.edu\/zh\/scientist\/martin-hetzer\/\">Martin Hetzer<\/a>, vice president and chief science officer of the Salk Institute and senior author of the paper. &#8220;When a cell devotes valuable resources to producing protein, other important functions may be neglected. Our work suggests that one driver of both abnormal and normal aging could be accelerated protein turnover.&#8221;<\/p>\n<figure id=\"attachment_14589\"  class=\"wp-caption alignright\"><img loading=\"lazy\" decoding=\"async\" width=\"300\" height=\"171\" class=\"img-responsive wp-image-14589 size-pr-300\" src=\"https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/08\/nucleoli-images-simple-2000-300x171.jpg\" alt=\"Nucleoli in the cell nucleus, stained bright magenta and cyan against the purple backdrop of the nucleus, are enlarged in the progeria cell (right) compared to the normal cell (left).\" srcset=\"https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/08\/nucleoli-images-simple-2000-300x171.jpg 300w, https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/08\/nucleoli-images-simple-2000-768x438.jpg 768w, https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/08\/nucleoli-images-simple-2000-1024x584.jpg 1024w, https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/08\/nucleoli-images-simple-2000-147x84.jpg 147w, https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/08\/nucleoli-images-simple-2000-458x261.jpg 458w, https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/08\/nucleoli-images-simple-2000-585x334.jpg 585w, https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/08\/nucleoli-images-simple-2000-553x315.jpg 553w, https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/08\/nucleoli-images-simple-2000-750x428.jpg 750w, https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/08\/nucleoli-images-simple-2000-945x539.jpg 945w, https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/08\/nucleoli-images-simple-2000.jpg 2000w\" sizes=\"auto, (max-width: 300px) 100vw, 300px\" \/><figcaption class=\"wp-caption-text\">Nucleoli in the cell nucleus, stained bright magenta and cyan against the purple backdrop of the nucleus, are enlarged in the progeria cell (right) compared to the normal cell (left). <\/p>\n<p> <a href=\"https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/08\/nucleoli-images-simple-2000.jpg\">Click here<\/a> for a high-resolution image.<\/p>\n<p> Credit: Salk Institute<\/figcaption><\/figure>\n<p>Hutchinson-Gilford progeria is a very rare genetic disease causing people to age 8 to 10 times faster than the rest of us and leading to an early death. The rare mutation occurs in one of the structural proteins in the cell nucleus, lamin A, but it has been unclear how a single defective protein in the nucleus causes the myriad rapid-aging features seen in the disease.<\/p>\n<p>Initially, Salk Staff Scientist Abigail Buchwalter, first author of the paper, was interested in whether the mutation was making the lamin A protein less stable and shorter lived. After measuring protein turnover in cultured cells from skin biopsies of both progeria sufferers and healthy people, she found that it wasn\u2019t just lamin A that was affected in the disease.<\/p>\n<p>&#8220;We analyzed all the proteins of the nucleus and instead of seeing rapid turnover in just mutant lamin A and maybe a few proteins associated with it, we saw a really broad shift in overall protein stability in the progeria cells,&#8221; says Buchwalter. &#8220;This indicated a change in protein metabolism that we hadn&#8217;t expected.&#8221;<\/p>\n<p>Along with the rapid turnover of proteins, the team found that the nucleolus, which makes protein-assembling structures called ribosomes, was enlarged in the prematurely aging cells compared to healthy cells.<\/p>\n<figure id=\"attachment_14588\"  class=\"wp-caption alignleft\"><img loading=\"lazy\" decoding=\"async\" width=\"300\" height=\"229\" class=\"img-responsive wp-image-14588 size-pr-300\" src=\"https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/08\/Martin-Hetzer_Abby-Buchwalter_Y49A9257e-300x229.jpg\" alt=\"\" srcset=\"https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/08\/Martin-Hetzer_Abby-Buchwalter_Y49A9257e-300x229.jpg 300w, https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/08\/Martin-Hetzer_Abby-Buchwalter_Y49A9257e-768x585.jpg 768w, https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/08\/Martin-Hetzer_Abby-Buchwalter_Y49A9257e-1024x780.jpg 1024w, https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/08\/Martin-Hetzer_Abby-Buchwalter_Y49A9257e-147x112.jpg 147w, https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/08\/Martin-Hetzer_Abby-Buchwalter_Y49A9257e-458x349.jpg 458w, https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/08\/Martin-Hetzer_Abby-Buchwalter_Y49A9257e-585x446.jpg 585w, https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/08\/Martin-Hetzer_Abby-Buchwalter_Y49A9257e-553x421.jpg 553w, https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/08\/Martin-Hetzer_Abby-Buchwalter_Y49A9257e-750x572.jpg 750w, https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/08\/Martin-Hetzer_Abby-Buchwalter_Y49A9257e-945x720.jpg 945w, https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/08\/Martin-Hetzer_Abby-Buchwalter_Y49A9257e.jpg 2000w\" sizes=\"auto, (max-width: 300px) 100vw, 300px\" \/><figcaption class=\"wp-caption-text\">From left: Martin Hetzer and Abigail Buchwalter <\/p>\n<p> <a href=\"https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/08\/Martin-Hetzer_Abby-Buchwalter_Y49A9257e.jpg\">Click here<\/a> for a high-resolution image <\/p>\n<p> Credit: Salk Institute<\/figcaption><\/figure>\n<p>Even more intriguing, the team found that nucleolus size increased with age in the healthy cells, suggesting that the size of the nucleolus could not only be a useful biomarker of aging, but potentially a target of therapies to counter both premature and normal aging.<\/p>\n<p>The work supports other research that appears in the same issue showing that decreasing protein synthesis extends lifespan in roundworms and mice. The Hetzer lab plans to continue studying how nucleolus size may serve as a reliable biomarker for aging.<\/p>\n<p>&#8220;We always assume that aging is a linear process, but we don&#8217;t know that for sure,\u201d says Hetzer, who also holds the Jesse and Caryl Philips Foundation Chair. \u201cA biomarker such as this that tracks aging would be very useful, and could open up new ways of studying and understanding aging in humans.&#8221;<\/p>\n<p>The work was funded by the <a href=\"https:\/\/www.nih.gov\/\" target=\"_blank\" rel=\"noopener\">National Institutes of Health<\/a>, the <a href=\"http:\/\/nomisfoundation.ch\/\" target=\"_blank\" rel=\"noopener\">Nomis Foundation<\/a>, and the <a href=\"http:\/\/glennfoundation.org\/\" target=\"_blank\" rel=\"noopener\">Glenn Center for Aging Research<\/a>.<\/p>","protected":false},"featured_media":14602,"template":"","faculty":[86],"disease-research":[146],"class_list":["post-14586","disclosure","type-disclosure","status-publish","has-post-thumbnail","hentry","faculty-martin-hetzer","disease-research-aging-and-regenerative-medicine"],"acf":[],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v27.3 - https:\/\/yoast.com\/product\/yoast-seo-wordpress\/ -->\n<title>Protein turnover could be clue to living longer - 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\/zh\/news-release\/protein-turnover-clue-living-longer\/\" \/>\n<meta property=\"og:locale\" content=\"zh_CN\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Protein turnover could be clue to living longer - Salk Institute for Biological Studies\" \/>\n<meta property=\"og:description\" content=\"LA JOLLA\u2014It may seem paradoxical, but studying what goes wrong in rare diseases can provide useful insights into normal health. 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