C. elegans expressing D76N β2-microglobulin: a model for in vivo screening of drug candidates targeting amyloidosis
The availability of a genetic model organism with which to study key molecular events underlying amyloidogenesis is crucial for elucidating the mechanism of the disease and the exploration of new therapeutic avenues. The natural human variant of β 2 -microglobulin (D76N β 2 -m) is associated with a...
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creator | Faravelli, Giulia Raimondi, Sara Marchese, Loredana Partridge, Frederick A. Soria, Cristina Mangione, P. Patrizia Canetti, Diana Perni, Michele Aprile, Francesco A. Zorzoli, Irene Di Schiavi, Elia Lomas, David A. Bellotti, Vittorio Sattelle, David B. Giorgetti, Sofia |
description | The availability of a genetic model organism with which to study key molecular events underlying amyloidogenesis is crucial for elucidating the mechanism of the disease and the exploration of new therapeutic avenues. The natural human variant of β
2
-microglobulin (D76N β
2
-m) is associated with a fatal familial form of systemic amyloidosis. Hitherto, no animal model has been available for studying
in vivo
the pathogenicity of this protein. We have established a transgenic
C. elegans
line, expressing the human D76N β
2
-m variant. Using the INVertebrate Automated Phenotyping Platform (INVAPP) and the algorithm Paragon, we were able to detect growth and motility impairment in D76N β
2
-m expressing worms. We also demonstrated the specificity of the β
2
-m variant in determining the pathological phenotype by rescuing the wild type phenotype when β
2
-m expression was inhibited by RNA interference (RNAi). Using this model, we have confirmed the efficacy of doxycycline, an inhibitor of the aggregation of amyloidogenic proteins, in rescuing the phenotype. In future, this
C. elegans
model, in conjunction with the INVAPP/Paragon system, offers the prospect of high-throughput chemical screening in the search for new drug candidates. |
doi_str_mv | 10.1038/s41598-019-56498-5 |
format | Article |
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2
-microglobulin (D76N β
2
-m) is associated with a fatal familial form of systemic amyloidosis. Hitherto, no animal model has been available for studying
in vivo
the pathogenicity of this protein. We have established a transgenic
C. elegans
line, expressing the human D76N β
2
-m variant. Using the INVertebrate Automated Phenotyping Platform (INVAPP) and the algorithm Paragon, we were able to detect growth and motility impairment in D76N β
2
-m expressing worms. We also demonstrated the specificity of the β
2
-m variant in determining the pathological phenotype by rescuing the wild type phenotype when β
2
-m expression was inhibited by RNA interference (RNAi). Using this model, we have confirmed the efficacy of doxycycline, an inhibitor of the aggregation of amyloidogenic proteins, in rescuing the phenotype. In future, this
C. elegans
model, in conjunction with the INVAPP/Paragon system, offers the prospect of high-throughput chemical screening in the search for new drug candidates.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-019-56498-5</identifier><identifier>PMID: 31882874</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>38/77 ; 38/89 ; 45/22 ; 45/23 ; 45/29 ; 45/44 ; 631/1647 ; 631/45 ; 64/11 ; 82 ; 82/1 ; 82/16 ; 82/29 ; Amyloidogenesis ; Amyloidosis ; Animal models ; Doxycycline ; Drug development ; Genotype & phenotype ; Humanities and Social Sciences ; Invertebrates ; multidisciplinary ; Pathogenicity ; Pathogens ; Phenotypes ; Phenotyping ; RNA-mediated interference ; Science ; Science (multidisciplinary) ; Worms ; β2 Microglobulin</subject><ispartof>Scientific reports, 2019-12, Vol.9 (1), p.1-10, Article 19960</ispartof><rights>The Author(s) 2019</rights><rights>2019. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c517t-e96064a9630cef0f46fe9a47ec70586be5e4b5786ba1f2f6ac53a4ce046bfd03</citedby><cites>FETCH-LOGICAL-c517t-e96064a9630cef0f46fe9a47ec70586be5e4b5786ba1f2f6ac53a4ce046bfd03</cites><orcidid>0000-0001-6236-4297 ; 0000-0002-0467-864X ; 0000-0001-6750-6450 ; 0000-0002-8179-6666 ; 0000-0001-9438-6511 ; 0000-0001-7593-8376</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6934621/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6934621/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,41096,42165,51551,53766,53768</link.rule.ids></links><search><creatorcontrib>Faravelli, Giulia</creatorcontrib><creatorcontrib>Raimondi, Sara</creatorcontrib><creatorcontrib>Marchese, Loredana</creatorcontrib><creatorcontrib>Partridge, Frederick A.</creatorcontrib><creatorcontrib>Soria, Cristina</creatorcontrib><creatorcontrib>Mangione, P. Patrizia</creatorcontrib><creatorcontrib>Canetti, Diana</creatorcontrib><creatorcontrib>Perni, Michele</creatorcontrib><creatorcontrib>Aprile, Francesco A.</creatorcontrib><creatorcontrib>Zorzoli, Irene</creatorcontrib><creatorcontrib>Di Schiavi, Elia</creatorcontrib><creatorcontrib>Lomas, David A.</creatorcontrib><creatorcontrib>Bellotti, Vittorio</creatorcontrib><creatorcontrib>Sattelle, David B.</creatorcontrib><creatorcontrib>Giorgetti, Sofia</creatorcontrib><title>C. elegans expressing D76N β2-microglobulin: a model for in vivo screening of drug candidates targeting amyloidosis</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><description>The availability of a genetic model organism with which to study key molecular events underlying amyloidogenesis is crucial for elucidating the mechanism of the disease and the exploration of new therapeutic avenues. The natural human variant of β
2
-microglobulin (D76N β
2
-m) is associated with a fatal familial form of systemic amyloidosis. Hitherto, no animal model has been available for studying
in vivo
the pathogenicity of this protein. We have established a transgenic
C. elegans
line, expressing the human D76N β
2
-m variant. Using the INVertebrate Automated Phenotyping Platform (INVAPP) and the algorithm Paragon, we were able to detect growth and motility impairment in D76N β
2
-m expressing worms. We also demonstrated the specificity of the β
2
-m variant in determining the pathological phenotype by rescuing the wild type phenotype when β
2
-m expression was inhibited by RNA interference (RNAi). Using this model, we have confirmed the efficacy of doxycycline, an inhibitor of the aggregation of amyloidogenic proteins, in rescuing the phenotype. In future, this
C. elegans
model, in conjunction with the INVAPP/Paragon system, offers the prospect of high-throughput chemical screening in the search for new drug candidates.</description><subject>38/77</subject><subject>38/89</subject><subject>45/22</subject><subject>45/23</subject><subject>45/29</subject><subject>45/44</subject><subject>631/1647</subject><subject>631/45</subject><subject>64/11</subject><subject>82</subject><subject>82/1</subject><subject>82/16</subject><subject>82/29</subject><subject>Amyloidogenesis</subject><subject>Amyloidosis</subject><subject>Animal models</subject><subject>Doxycycline</subject><subject>Drug development</subject><subject>Genotype & phenotype</subject><subject>Humanities and Social Sciences</subject><subject>Invertebrates</subject><subject>multidisciplinary</subject><subject>Pathogenicity</subject><subject>Pathogens</subject><subject>Phenotypes</subject><subject>Phenotyping</subject><subject>RNA-mediated interference</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><subject>Worms</subject><subject>β2 Microglobulin</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kctu1TAURSMEolXpDzCyxIRJit-JGSChS3lIFUw6txznOLhy7IudXLW_xYf0m3C4Fa8BnnhLZ-2tY--meU7wBcGsf1U4EapvMVGtkLwq8ag5pZiLljJKH_-hT5rzUm5wPYIqTtTT5oSRvqd9x0-bZXeBIMBkYkFwu89Qio8TetfJz-j-O21nb3OaQhrW4ONrZNCcRgjIpYx8RAd_SKjYDBA3V3JozOuErImjH80CBS0mT7BsQzPfheTHVHx51jxxJhQ4f7jPmuv3l9e7j-3Vlw-fdm-vWitIt7SgJJbcKMmwBYcdlw6U4R3YDoteDiCAD6KryhBHnTRWMMMtYC4HN2J21rw5xu7XYYbRQlyyCXqf_WzynU7G678n0X_VUzpoqRiXlNSAlw8BOX1boSx69sVCCCZCWoumjBHKVcc29MU_6E1ac6yv2yispJKUVooeqfqppWRwv5YhWG-16mOtutaqf9aqRTWxo6lUOE6Qf0f_x_UDHzWmPg</recordid><startdate>20191227</startdate><enddate>20191227</enddate><creator>Faravelli, Giulia</creator><creator>Raimondi, Sara</creator><creator>Marchese, Loredana</creator><creator>Partridge, Frederick A.</creator><creator>Soria, Cristina</creator><creator>Mangione, P. 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Patrizia</creatorcontrib><creatorcontrib>Canetti, Diana</creatorcontrib><creatorcontrib>Perni, Michele</creatorcontrib><creatorcontrib>Aprile, Francesco A.</creatorcontrib><creatorcontrib>Zorzoli, Irene</creatorcontrib><creatorcontrib>Di Schiavi, Elia</creatorcontrib><creatorcontrib>Lomas, David A.</creatorcontrib><creatorcontrib>Bellotti, Vittorio</creatorcontrib><creatorcontrib>Sattelle, David B.</creatorcontrib><creatorcontrib>Giorgetti, Sofia</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>ProQuest Central (New)</collection><collection>ProQuest One Academic (New)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest Health & Medical Research Collection</collection><collection>ProQuest One Academic Middle East (New)</collection><collection>ProQuest One Health & Nursing</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Applied & Life Sciences</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Faravelli, Giulia</au><au>Raimondi, Sara</au><au>Marchese, Loredana</au><au>Partridge, Frederick A.</au><au>Soria, Cristina</au><au>Mangione, P. Patrizia</au><au>Canetti, Diana</au><au>Perni, Michele</au><au>Aprile, Francesco A.</au><au>Zorzoli, Irene</au><au>Di Schiavi, Elia</au><au>Lomas, David A.</au><au>Bellotti, Vittorio</au><au>Sattelle, David B.</au><au>Giorgetti, Sofia</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>C. elegans expressing D76N β2-microglobulin: a model for in vivo screening of drug candidates targeting amyloidosis</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><date>2019-12-27</date><risdate>2019</risdate><volume>9</volume><issue>1</issue><spage>1</spage><epage>10</epage><pages>1-10</pages><artnum>19960</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>The availability of a genetic model organism with which to study key molecular events underlying amyloidogenesis is crucial for elucidating the mechanism of the disease and the exploration of new therapeutic avenues. The natural human variant of β
2
-microglobulin (D76N β
2
-m) is associated with a fatal familial form of systemic amyloidosis. Hitherto, no animal model has been available for studying
in vivo
the pathogenicity of this protein. We have established a transgenic
C. elegans
line, expressing the human D76N β
2
-m variant. Using the INVertebrate Automated Phenotyping Platform (INVAPP) and the algorithm Paragon, we were able to detect growth and motility impairment in D76N β
2
-m expressing worms. We also demonstrated the specificity of the β
2
-m variant in determining the pathological phenotype by rescuing the wild type phenotype when β
2
-m expression was inhibited by RNA interference (RNAi). Using this model, we have confirmed the efficacy of doxycycline, an inhibitor of the aggregation of amyloidogenic proteins, in rescuing the phenotype. In future, this
C. elegans
model, in conjunction with the INVAPP/Paragon system, offers the prospect of high-throughput chemical screening in the search for new drug candidates.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>31882874</pmid><doi>10.1038/s41598-019-56498-5</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0001-6236-4297</orcidid><orcidid>https://orcid.org/0000-0002-0467-864X</orcidid><orcidid>https://orcid.org/0000-0001-6750-6450</orcidid><orcidid>https://orcid.org/0000-0002-8179-6666</orcidid><orcidid>https://orcid.org/0000-0001-9438-6511</orcidid><orcidid>https://orcid.org/0000-0001-7593-8376</orcidid><oa>free_for_read</oa></addata></record> |
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source | Nature Free; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Alma/SFX Local Collection; Free Full-Text Journals in Chemistry; Springer Nature OA Free Journals |
subjects | 38/77 38/89 45/22 45/23 45/29 45/44 631/1647 631/45 64/11 82 82/1 82/16 82/29 Amyloidogenesis Amyloidosis Animal models Doxycycline Drug development Genotype & phenotype Humanities and Social Sciences Invertebrates multidisciplinary Pathogenicity Pathogens Phenotypes Phenotyping RNA-mediated interference Science Science (multidisciplinary) Worms β2 Microglobulin |
title | C. elegans expressing D76N β2-microglobulin: a model for in vivo screening of drug candidates targeting amyloidosis |
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