{"id":15604,"date":"2017-12-07T00:00:52","date_gmt":"2017-12-07T08:00:52","guid":{"rendered":"https:\/\/vermont.salk.edu\/?post_type=disclosure&#038;p=15604"},"modified":"2024-01-30T15:25:44","modified_gmt":"2024-01-30T23:25:44","slug":"salk-scientists-modify-crispr-epigenetically-treat-diabetes-kidney-disease-muscular-dystrophy","status":"publish","type":"disclosure","link":"https:\/\/www.salk.edu\/de\/news-release\/salk-scientists-modify-crispr-epigenetically-treat-diabetes-kidney-disease-muscular-dystrophy\/","title":{"rendered":"Salk scientists modify CRISPR to epigenetically treat diabetes, kidney disease, muscular dystrophy"},"content":{"rendered":"<p>LA JOLLA\u2014Salk scientists have created a new version of the CRISPR\/Cas9 genome editing technology that allows them to activate genes without creating breaks in the DNA, potentially circumventing a major hurdle to using gene editing technologies to treat human diseases.<\/p>\n<div class=\"row\" style=\"\"><div class=\"col-md-12 col-md-push-0\"><div class=\"video-anchor\" id=\"video-zhS0CZprpaA\"><\/div><div class=\"embed-responsive embed-responsive-16by9\"> <iframe class=\"embed-responsive-item\" src=\"\/\/www.youtube.com\/embed\/zhS0CZprpaA?rel=0\" webkitallowfullscreen mozallowfullscreen allowfullscreen><\/iframe><\/div><!-- .embed-responsive --><\/div><!-- .col-md-*size --><\/div><!-- .\/row -->\n<p>Most CRISPR\/Cas9 systems work by creating \u201cdouble-strand breaks\u201d (DSBs) in regions of the genome targeted for editing or for deletion, but many researchers are opposed to creating such breaks in the DNA of living humans. As a proof of concept, the Salk group used their new approach to treat several diseases, including diabetes, acute kidney disease, and muscular dystrophy, in mouse models.<\/p>\n<p>\u201cAlthough many studies have demonstrated that CRISPR\/Cas9 can be applied as a powerful tool for gene therapy, there are growing concerns regarding unwanted mutations generated by the double-strand breaks through this technology,\u201d says <a href=\"https:\/\/www.salk.edu\/de\/scientist\/juan-carlos-izpisua-belmonte\/\">Juan Carlos Izpisua Belmonte<\/a>, a professor in Salk\u2019s Gene Expression Laboratory and senior author of the new paper, published in <a href=\"http:\/\/www.cell.com\/cell\/fulltext\/S0092-8674(17)31247-3\"><em>Zelle<\/em><\/a> on December 7, 2017. \u201cWe were able to get around that concern.\u201d<\/p>\n<figure id=\"attachment_15614\"  class=\"wp-caption alignright\"><img loading=\"lazy\" decoding=\"async\" width=\"300\" height=\"225\" class=\"img-responsive wp-image-15614 size-pr-300\" src=\"https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/12\/Muscle-Fst-Cas9-mouse-300x225.png\" alt=\"\" srcset=\"https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/12\/Muscle-Fst-Cas9-mouse-300x225.png 300w, https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/12\/Muscle-Fst-Cas9-mouse-768x576.png 768w, https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/12\/Muscle-Fst-Cas9-mouse-1024x768.png 1024w, https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/12\/Muscle-Fst-Cas9-mouse-147x110.png 147w, https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/12\/Muscle-Fst-Cas9-mouse-458x343.png 458w, https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/12\/Muscle-Fst-Cas9-mouse-585x439.png 585w, https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/12\/Muscle-Fst-Cas9-mouse-553x415.png 553w, https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/12\/Muscle-Fst-Cas9-mouse-750x562.png 750w, https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/12\/Muscle-Fst-Cas9-mouse-945x709.png 945w, https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/12\/Muscle-Fst-Cas9-mouse.png 1687w\" sizes=\"auto, (max-width: 300px) 100vw, 300px\" \/><figcaption class=\"wp-caption-text\">The Belmonte lab&#8217;s advanced <em>in vivo<\/em> Cas9-based epigenetic gene activation system enhances skeletal muscle mass (top) and fiber size growth (bottom) in a treated mouse (right) compared with an independent control (left). The fluorescent microscopy images at bottom show purple staining of the laminin glycoprotein in tibialis anterior muscle fibers. <\/p>\n<p> <a href=\"https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/12\/Muscle-Fst-Cas9-mouse.png\">Klicken Sie hier<\/a> f\u00fcr ein hochaufl\u00f6sendes Bild. <\/p>\n<p> Kredit: Salk Institut<\/figcaption><\/figure>\n<p>In the original CRISPR\/Cas9 system, the enzyme Cas9 is coupled with guide RNAs that target it to the right spot in the genome to create DSBs. Recently, some researchers have started using a \u201cdead\u201d form of Cas9 (dCas9), which can still target specific places in the genome, but no longer cuts DNA. Instead, dCas9 has been coupled with transcriptional activation domains\u2014molecular switches\u2014that turn on targeted genes. But the resulting protein\u2014dCas9 attached to the activator switches\u2014is too large and bulky to fit into the vehicle typically used to deliver these kinds of therapies to cells in living organisms, namely adeno-associated viruses (AAVs). The lack of an efficient delivery system makes it very difficult to use this tool in clinical applications.<\/p>\n<p>Izpisua Belmonte\u2019s team combined Cas9\/dCas9 with a range of different activator switches to uncover a combination that worked even when the proteins were not fused to one another. In other words, Cas9 or dCas9 was packaged into one AAV, and the switches and guide RNAs were packaged into another. They also optimized the guide RNAs to make sure all the pieces ended up at the desired place in the genome, and that the targeted gene was strongly activated.<\/p>\n<p>\u201cThe components all work together in the organism to influence endogenous genes,\u201d says Hsin-Kai (Ken) Liao, a staff researcher in the Izpisua Belmonte lab and co\u2013first author of the new paper. In this way, the technology operates epigenetically, meaning it influences gene activity without changing the DNA sequence.<\/p>\n<figure id=\"attachment_15613\"  class=\"wp-caption alignleft\"><img loading=\"lazy\" decoding=\"async\" width=\"300\" height=\"200\" class=\"img-responsive wp-image-15613 size-pr-300\" src=\"https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/12\/Belmonte-lab-CRISPR-epigenetics-300x200.jpg\" alt=\"Hsin-Kai (Ken) Liao, Juan Carlos Izpisua Belmonte and Fumiyuki Hatanaka\" srcset=\"https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/12\/Belmonte-lab-CRISPR-epigenetics-300x200.jpg 300w, https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/12\/Belmonte-lab-CRISPR-epigenetics-768x512.jpg 768w, https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/12\/Belmonte-lab-CRISPR-epigenetics-1024x683.jpg 1024w, https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/12\/Belmonte-lab-CRISPR-epigenetics-147x98.jpg 147w, https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/12\/Belmonte-lab-CRISPR-epigenetics-458x305.jpg 458w, https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/12\/Belmonte-lab-CRISPR-epigenetics-585x390.jpg 585w, https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/12\/Belmonte-lab-CRISPR-epigenetics-553x369.jpg 553w, https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/12\/Belmonte-lab-CRISPR-epigenetics-750x500.jpg 750w, https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/12\/Belmonte-lab-CRISPR-epigenetics-945x630.jpg 945w\" sizes=\"auto, (max-width: 300px) 100vw, 300px\" \/><figcaption class=\"wp-caption-text\">From left: Hsin-Kai (Ken) Liao, Juan Carlos Izpisua Belmonte and Fumiyuki Hatanaka <\/p>\n<p> <a href=\"https:\/\/www.salk.edu\/wp-content\/uploads\/2017\/12\/Belmonte-lab-CRISPR-epigenetics.jpg\">Klicken Sie hier<\/a> f\u00fcr ein hochaufl\u00f6sendes Bild. <\/p>\n<p> Kredit: Salk Institut<\/figcaption><\/figure>\n<p>To test the method, the researchers used mouse models of acute kidney injury, type 1 diabetes and a form of muscular dystrophy. In each case, they engineered their CRISPR\/Cas9 system to boost the expression of an endogenous gene that could potentially reverse disease symptoms. In the case of kidney disease, they activated two genes known to be involved in kidney function, and observed not only increased levels of the proteins associated with those genes, but improved kidney function following an acute injury. For type 1 diabetes, they aimed to boost the activity of genes that could generate insulin-producing cells. Once again, the treatment worked, lowering blood glucose levels in a mouse model of diabetes. For muscular dystrophy, the researchers expressed genes that have been previously shown to reverse disease symptoms, including one particularly large gene that cannot easily be delivered via traditional virus-mediated gene therapies.<\/p>\n<p>\u201cWe were very excited when we saw the results in mice,\u201d adds Fumiyuki Hatanaka, a research associate in the lab and co\u2013first author of the paper. \u201cWe can induce gene activation and at the same time see physiological changes.\u201d<\/p>\n<p>Izpisua Belmonte\u2019s team is now working to improve the specificity of their system and to apply it to more cell types and organs to treat a wider range of human diseases, as well as to rejuvenate specific organs and to reverse the aging process and age-related conditions such as hearing loss and macular degeneration. More safety tests will be needed before human trials, they say.<\/p>\n<p>Other researchers on the study were Toshikazu Araoka, Pradeep Reddy, Min-Zu Wu, Takayoshi Yamauchi, Masahiro Sakurai, David O\u2019Keefe, and Concepcion Rodriguez Esteban of the Salk Institute; Yinghui Sui, Cheng-Jang Wu, and Li-Fan Lu of the University of California, San Diego; Estrella Nu\u00f1ez of Universidad Cat\u00f3lica; Pedro Guill\u00e9n of Fundaci\u00f3n Pedro Guill\u00e9n; and Josep Campistol of Hospital Clinic of Barcelona.<\/p>\n<p>The work and the researchers involved were supported by grants from the Uehara Memorial Foundation, the Moxie Foundation, The Leona M. and Harry B. Helmsley Charitable Trust, the G. Harold and Leila Y. Mathers Charitable Foundation, Fundaci\u00f3n Dr. Pedro Guill\u00e9n, Asociaci\u00f3n de Futbolistas Espa\u00f1oles (AFE), Universidad Cat\u00f3lica de San Antonio de Murcia (UCAM), the National Institutes of Health, Howard Hughes Medical Institute, and a Calouste Gulbenkkian Foundation Fellowship.<\/p>","protected":false},"featured_media":15605,"template":"","faculty":[85],"disease-research":[173,165],"class_list":["post-15604","disclosure","type-disclosure","status-publish","has-post-thumbnail","hentry","faculty-juan-carlos-izpisua-belmonte","disease-research-diabetes-type-1","disease-research-diabetes-type-2"],"acf":[],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v27.3 - https:\/\/yoast.com\/product\/yoast-seo-wordpress\/ -->\n<title>Salk scientists modify CRISPR to epigenetically treat diabetes, kidney disease, muscular dystrophy - 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\/salk-scientists-modify-crispr-epigenetically-treat-diabetes-kidney-disease-muscular-dystrophy\/\" \/>\n<meta property=\"og:locale\" content=\"de_DE\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Salk scientists modify CRISPR to epigenetically treat diabetes, kidney disease, muscular dystrophy - 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Campistol, Concepcion Rodriguez Esteban, Juan Carlos Izpisua Belmonte","paper_title":"<em>In Vivo<\/em> Target Gene Activation via CRISPR\/Cas9-Mediated Trans-Epigenetic Modulation","subhead":"Approach could also be applied to reversing aging and age-related diseases such as hearing loss and macular degeneration","home_photo":"","listing_photo":"","legacy_boilerplate":[],"hide_boilerplate":[],"disable_date":false,"listing_excerpt":"","descriptive_blurb":"","has_journal_cover":false,"poster_quote":"","doi":"","og_image_override":false},"_links":{"self":[{"href":"https:\/\/www.salk.edu\/de\/wp-json\/wp\/v2\/disclosure\/15604","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/www.salk.edu\/de\/wp-json\/wp\/v2\/disclosure"}],"about":[{"href":"https:\/\/www.salk.edu\/de\/wp-json\/wp\/v2\/types\/disclosure"}],"version-history":[{"count":14,"href":"https:\/\/www.salk.edu\/de\/wp-json\/wp\/v2\/disclosure\/15604\/revisions"}],"predecessor-version":[{"id":15696,"href":"https:\/\/www.salk.edu\/de\/wp-json\/wp\/v2\/disclosure\/15604\/revisions\/15696"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/www.salk.edu\/de\/wp-json\/wp\/v2\/media\/15605"}],"wp:attachment":[{"href":"https:\/\/www.salk.edu\/de\/wp-json\/wp\/v2\/media?parent=15604"}],"wp:term":[{"taxonomy":"faculty","embeddable":true,"href":"https:\/\/www.salk.edu\/de\/wp-json\/wp\/v2\/faculty?post=15604"},{"taxonomy":"disease-research","embeddable":true,"href":"https:\/\/www.salk.edu\/de\/wp-json\/wp\/v2\/disease-research?post=15604"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}