Behavioral characterization of a CRISPR-generated TRPA1 knockout rat in models of pain, itch, and asthma
Identifieur interne : 000206 ( an2020/Analysis ); précédent : 000205; suivant : 000207Behavioral characterization of a CRISPR-generated TRPA1 knockout rat in models of pain, itch, and asthma
Auteurs : Rebecca M. Reese [États-Unis] ; Michelle Dourado [États-Unis] ; Keith Anderson [États-Unis] ; S Ren Warming [États-Unis] ; Kimberly L. Stark [États-Unis] ; Alessia Balestrini [États-Unis] ; Eric Suto [États-Unis] ; Wyne Lee [États-Unis] ; Lorena Riol-Blanco [États-Unis] ; Shannon D. Shields [États-Unis] ; David H. Hackos [États-Unis]Source :
- Scientific Reports [ 2045-2322 ] ; 2020.
Abstract
The transient receptor potential (TRP) superfamily of ion channels has garnered significant attention by the pharmaceutical industry. In particular, TRP channels showing high levels of expression in sensory neurons such as TRPV1, TRPA1, and TRPM8, have been considered as targets for indications where sensory neurons play a fundamental role, such as pain, itch, and asthma. Modeling these indications in rodents is challenging, especially in mice. The rat is the preferred species for pharmacological studies in pain, itch, and asthma, but until recently, genetic manipulation of the rat has been technically challenging. Here, using CRISPR technology, we have generated a TRPA1 KO rat to enable more sophisticated modeling of pain, itch, and asthma. We present a detailed phenotyping of the TRPA1 KO rat in models of pain, itch, and asthma that have previously only been investigated in the mouse. With the exception of nociception induced by direct TRPA1 activation, we have found that the TRPA1 KO rat shows apparently normal behavioral responses in multiple models of pain and itch. Immune cell infiltration into the lung in the rat OVA model of asthma, on the other hand, appears to be dependent on TRPA1, similar to was has been observed in TRPA1 KO mice. Our hope is that the TRPA1 KO rat will become a useful tool in further studies of TRPA1 as a drug target.
Url:
DOI: 10.1038/s41598-020-57936-5
PubMed: 31969645
PubMed Central: 6976688
Affiliations:
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PMC:6976688Le document en format XML
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Shields</name><affiliation wicri:level="2"><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 0534 4718</institution-id><institution-id institution-id-type="GRID">grid.418158.1</institution-id><institution>Department of Neuroscience,</institution><institution>Genentech, 1 DNA Way,</institution></institution-wrap>South San Francisco, CA 94080 USA</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>South San Francisco</wicri:cityArea></affiliation></author><author><name sortKey="Hackos, David H" sort="Hackos, David H" uniqKey="Hackos D" first="David H." last="Hackos">David H. Hackos</name><affiliation wicri:level="2"><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 0534 4718</institution-id><institution-id institution-id-type="GRID">grid.418158.1</institution-id><institution>Department of Neuroscience,</institution><institution>Genentech, 1 DNA Way,</institution></institution-wrap>South San Francisco, CA 94080 USA</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>South San Francisco</wicri:cityArea></affiliation></author></analytic><series><title level="j">Scientific Reports</title><idno type="eISSN">2045-2322</idno><imprint><date when="2020">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="Par1">The transient receptor potential (TRP) superfamily of ion channels has garnered significant attention by the pharmaceutical industry. In particular, TRP channels showing high levels of expression in sensory neurons such as TRPV1, TRPA1, and TRPM8, have been considered as targets for indications where sensory neurons play a fundamental role, such as pain, itch, and asthma. Modeling these indications in rodents is challenging, especially in mice. The rat is the preferred species for pharmacological studies in pain, itch, and asthma, but until recently, genetic manipulation of the rat has been technically challenging. Here, using CRISPR technology, we have generated a TRPA1 KO rat to enable more sophisticated modeling of pain, itch, and asthma. We present a detailed phenotyping of the TRPA1 KO rat in models of pain, itch, and asthma that have previously only been investigated in the mouse. With the exception of nociception induced by direct TRPA1 activation, we have found that the TRPA1 KO rat shows apparently normal behavioral responses in multiple models of pain and itch. Immune cell infiltration into the lung in the rat OVA model of asthma, on the other hand, appears to be dependent on TRPA1, similar to was has been observed in TRPA1 KO mice. Our hope is that the TRPA1 KO rat will become a useful tool in further studies of TRPA1 as a drug target.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Nagata, K" uniqKey="Nagata K">K Nagata</name></author><author><name sortKey="Duggan, A" uniqKey="Duggan A">A Duggan</name></author><author><name sortKey="Kumar, G" uniqKey="Kumar G">G Kumar</name></author><author><name sortKey="Garcia A Overos, J" uniqKey="Garcia A Overos J">J García-Añoveros</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Story, Gm" uniqKey="Story G">GM Story</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Bandell, M" uniqKey="Bandell M">M Bandell</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Bautista, Dm" uniqKey="Bautista D">DM Bautista</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Bessac, Bf" uniqKey="Bessac B">BF 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uniqKey="Pogrel J">JW Pogrel</name></author><author><name sortKey="Chung, Jm" uniqKey="Chung J">JM Chung</name></author><author><name sortKey="Yaksh, Tl" uniqKey="Yaksh T">TL Yaksh</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Californie</li></region></list><tree><country name="États-Unis"><region name="Californie"><name sortKey="Reese, Rebecca M" sort="Reese, Rebecca M" uniqKey="Reese R" first="Rebecca M." last="Reese">Rebecca M. Reese</name></region><name sortKey="Anderson, Keith" sort="Anderson, Keith" uniqKey="Anderson K" first="Keith" last="Anderson">Keith Anderson</name><name sortKey="Balestrini, Alessia" sort="Balestrini, Alessia" uniqKey="Balestrini A" first="Alessia" last="Balestrini">Alessia Balestrini</name><name sortKey="Dourado, Michelle" sort="Dourado, Michelle" uniqKey="Dourado M" first="Michelle" last="Dourado">Michelle Dourado</name><name sortKey="Hackos, David H" sort="Hackos, David H" uniqKey="Hackos D" first="David H." last="Hackos">David H. Hackos</name><name sortKey="Lee, Wyne" sort="Lee, Wyne" uniqKey="Lee W" first="Wyne" last="Lee">Wyne Lee</name><name sortKey="Riol Blanco, Lorena" sort="Riol Blanco, Lorena" uniqKey="Riol Blanco L" first="Lorena" last="Riol-Blanco">Lorena Riol-Blanco</name><name sortKey="Shields, Shannon D" sort="Shields, Shannon D" uniqKey="Shields S" first="Shannon D." last="Shields">Shannon D. Shields</name><name sortKey="Stark, Kimberly L" sort="Stark, Kimberly L" uniqKey="Stark K" first="Kimberly L." last="Stark">Kimberly L. Stark</name><name sortKey="Suto, Eric" sort="Suto, Eric" uniqKey="Suto E" first="Eric" last="Suto">Eric Suto</name><name sortKey="Warming, S Ren" sort="Warming, S Ren" uniqKey="Warming S" first="S Ren" last="Warming">S Ren Warming</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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