Inhibition of the glutamine transporter SNAT1 confers neuroprotection in mice by modulating the mTOR-autophagy system
Identifieur interne : 000A50 ( Ncbi/Curation ); précédent : 000A49; suivant : 000A51Inhibition of the glutamine transporter SNAT1 confers neuroprotection in mice by modulating the mTOR-autophagy system
Auteurs : Daisuke Yamada [Japon] ; Kenji Kawabe [Japon] ; Ikue Tosa [Japon] ; Shunpei Tsukamoto [Japon] ; Ryota Nakazato ; Miki Kou ; Koichi Fujikawa ; Saki Nakamura ; Mitsuaki Ono [Japon] ; Toshitaka Oohashi [Japon] ; Mari Kaneko ; Shioi Go ; Eiichi Hinoi ; Yukio Yoneda ; Takeshi Takarada [Japon]Source :
- Communications Biology [ 2399-3642 ] ; 2019.
Abstract
The pathophysiological role of mammalian target of rapamycin complex 1 (mTORC1) in neurodegenerative diseases is established, but possible therapeutic targets responsible for its activation in neurons must be explored. Here we identified solute carrier family 38a member 1 (SNAT1,
Url:
DOI: 10.1038/s42003-019-0582-4
PubMed: 31552299
PubMed Central: 6751179
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Ryota Nakazato<affiliation><nlm:aff id="Aff2"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 2308 3329</institution-id><institution-id institution-id-type="GRID">grid.9707.9</institution-id><institution>Laboratory of Molecular Pharmacology, Division of Pharmaceutical Sciences,</institution><institution>Kanazawa University Graduate School,</institution></institution-wrap>Kanazawa, Ishikawa 920-1192 Japan</nlm:aff><wicri:noCountry code="subfield">Ishikawa 920-1192 Japan</wicri:noCountry></affiliation><affiliation><nlm:aff id="Aff2"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 2308 3329</institution-id><institution-id institution-id-type="GRID">grid.9707.9</institution-id><institution>Laboratory of Molecular Pharmacology, Division of Pharmaceutical Sciences,</institution><institution>Kanazawa University Graduate School,</institution></institution-wrap>Kanazawa, Ishikawa 920-1192 Japan</nlm:aff><wicri:noCountry code="subfield">Ishikawa 920-1192 Japan</wicri:noCountry></affiliation><affiliation><nlm:aff id="Aff2"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 2308 3329</institution-id><institution-id institution-id-type="GRID">grid.9707.9</institution-id><institution>Laboratory of Molecular Pharmacology, Division of Pharmaceutical Sciences,</institution><institution>Kanazawa University Graduate School,</institution></institution-wrap>Kanazawa, Ishikawa 920-1192 Japan</nlm:aff><wicri:noCountry code="subfield">Ishikawa 920-1192 Japan</wicri:noCountry></affiliation><affiliation><nlm:aff id="Aff2"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 2308 3329</institution-id><institution-id institution-id-type="GRID">grid.9707.9</institution-id><institution>Laboratory of Molecular Pharmacology, Division of Pharmaceutical Sciences,</institution><institution>Kanazawa University Graduate School,</institution></institution-wrap>Kanazawa, Ishikawa 920-1192 Japan</nlm:aff><wicri:noCountry code="subfield">Ishikawa 920-1192 Japan</wicri:noCountry></affiliation><affiliation><nlm:aff id="Aff4"><institution-wrap><institution-id institution-id-type="ISNI">0000000094465255</institution-id><institution-id institution-id-type="GRID">grid.7597.c</institution-id><institution>Laboratory for Animal Resource Development Unit and Genetic Engineering Team,</institution><institution>RIKEN Center for Life Science Technologies,</institution></institution-wrap>2-2-3 Minatojima Minami, Chuou-ku, Kobe, Hyogo 650-0047 Japan</nlm:aff><wicri:noCountry code="subfield">Hyogo 650-0047 Japan</wicri:noCountry></affiliation><affiliation><nlm:aff id="Aff4"><institution-wrap><institution-id institution-id-type="ISNI">0000000094465255</institution-id><institution-id institution-id-type="GRID">grid.7597.c</institution-id><institution>Laboratory for Animal Resource Development Unit and Genetic Engineering Team,</institution><institution>RIKEN Center for Life Science Technologies,</institution></institution-wrap>2-2-3 Minatojima Minami, Chuou-ku, Kobe, Hyogo 650-0047 Japan</nlm:aff><wicri:noCountry code="subfield">Hyogo 650-0047 Japan</wicri:noCountry></affiliation><affiliation><nlm:aff id="Aff2"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 2308 3329</institution-id><institution-id institution-id-type="GRID">grid.9707.9</institution-id><institution>Laboratory of Molecular Pharmacology, Division of Pharmaceutical Sciences,</institution><institution>Kanazawa University Graduate School,</institution></institution-wrap>Kanazawa, Ishikawa 920-1192 Japan</nlm:aff><wicri:noCountry code="subfield">Ishikawa 920-1192 Japan</wicri:noCountry></affiliation><affiliation><nlm:aff id="Aff2"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 2308 3329</institution-id><institution-id institution-id-type="GRID">grid.9707.9</institution-id><institution>Laboratory of Molecular Pharmacology, Division of Pharmaceutical Sciences,</institution><institution>Kanazawa University Graduate School,</institution></institution-wrap>Kanazawa, Ishikawa 920-1192 Japan</nlm:aff><wicri:noCountry code="subfield">Ishikawa 920-1192 Japan</wicri:noCountry></affiliation>Le document en format XML
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1302 4472</institution-id><institution-id institution-id-type="GRID">grid.261356.5</institution-id><institution>Department of Molecular Biology and Biochemistry,</institution><institution>Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences,</institution></institution-wrap>Okayama, 700-8558 Japan</nlm:aff><country xml:lang="fr">Japon</country><wicri:regionArea>Okayama</wicri:regionArea></affiliation></author><author><name sortKey="Kaneko, Mari" sort="Kaneko, Mari" uniqKey="Kaneko M" first="Mari" last="Kaneko">Mari Kaneko</name><affiliation><nlm:aff id="Aff4"><institution-wrap><institution-id institution-id-type="ISNI">0000000094465255</institution-id><institution-id institution-id-type="GRID">grid.7597.c</institution-id><institution>Laboratory for Animal Resource Development Unit and Genetic Engineering Team,</institution><institution>RIKEN Center for Life Science Technologies,</institution></institution-wrap>2-2-3 Minatojima Minami, Chuou-ku, Kobe, Hyogo 650-0047 Japan</nlm:aff><wicri:noCountry code="subfield">Hyogo 650-0047 Japan</wicri:noCountry></affiliation></author><author><name sortKey="Go, Shioi" sort="Go, Shioi" uniqKey="Go S" first="Shioi" last="Go">Shioi Go</name><affiliation><nlm:aff id="Aff4"><institution-wrap><institution-id institution-id-type="ISNI">0000000094465255</institution-id><institution-id institution-id-type="GRID">grid.7597.c</institution-id><institution>Laboratory for Animal Resource Development Unit and Genetic Engineering Team,</institution><institution>RIKEN Center for Life Science Technologies,</institution></institution-wrap>2-2-3 Minatojima Minami, Chuou-ku, Kobe, Hyogo 650-0047 Japan</nlm:aff><wicri:noCountry code="subfield">Hyogo 650-0047 Japan</wicri:noCountry></affiliation></author><author><name sortKey="Hinoi, Eiichi" sort="Hinoi, Eiichi" uniqKey="Hinoi E" first="Eiichi" last="Hinoi">Eiichi Hinoi</name><affiliation><nlm:aff id="Aff2"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 2308 3329</institution-id><institution-id institution-id-type="GRID">grid.9707.9</institution-id><institution>Laboratory of Molecular Pharmacology, Division of Pharmaceutical Sciences,</institution><institution>Kanazawa University Graduate School,</institution></institution-wrap>Kanazawa, Ishikawa 920-1192 Japan</nlm:aff><wicri:noCountry code="subfield">Ishikawa 920-1192 Japan</wicri:noCountry></affiliation></author><author><name sortKey="Yoneda, Yukio" sort="Yoneda, Yukio" uniqKey="Yoneda Y" first="Yukio" last="Yoneda">Yukio Yoneda</name><affiliation><nlm:aff id="Aff2"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 2308 3329</institution-id><institution-id institution-id-type="GRID">grid.9707.9</institution-id><institution>Laboratory of Molecular Pharmacology, Division of Pharmaceutical Sciences,</institution><institution>Kanazawa University Graduate School,</institution></institution-wrap>Kanazawa, Ishikawa 920-1192 Japan</nlm:aff><wicri:noCountry code="subfield">Ishikawa 920-1192 Japan</wicri:noCountry></affiliation></author><author><name sortKey="Takarada, Takeshi" sort="Takarada, Takeshi" uniqKey="Takarada T" first="Takeshi" last="Takarada">Takeshi Takarada</name><affiliation wicri:level="1"><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 1302 4472</institution-id><institution-id institution-id-type="GRID">grid.261356.5</institution-id><institution>Department of Regenerative Science,</institution><institution>Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences,</institution></institution-wrap>Okayama, 700-8558 Japan</nlm:aff><country xml:lang="fr">Japon</country><wicri:regionArea>Okayama</wicri:regionArea></affiliation></author></analytic><series><title level="j">Communications Biology</title><idno type="eISSN">2399-3642</idno><imprint><date when="2019">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="Par1">The pathophysiological role of mammalian target of rapamycin complex 1 (mTORC1) in neurodegenerative diseases is established, but possible therapeutic targets responsible for its activation in neurons must be explored. Here we identified solute carrier family 38a member 1 (SNAT1, <italic>Slc38a1</italic>) as a positive regulator of mTORC1 in neurons. <italic>Slc38a1</italic><sup><italic>flox/flox</italic></sup> and <italic>Synapsin I-Cre</italic> mice were crossed to generate mutant mice in which <italic>Slc38a1</italic> was selectively deleted in neurons. Measurement of 2,3,5-triphenyltetrazolium chloride (TTC) or the MAP2-negative area in a mouse model of middle cerebral artery occlusion (MCAO) revealed that <italic>Slc38a1</italic> deficiency decreased infarct size. We found a transient increase in the phosphorylation of p70S6k1 (pp70S6k1) and a suppressive effect of rapamycin on infarct size in MCAO mice. Autophagy inhibitors completely mitigated the suppressive effect of SNAT1 deficiency on neuronal cell death under in vitro stroke culture conditions. These results demonstrate that SNAT1 promoted ischemic brain damage via mTOR-autophagy system.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Nixon, Ra" uniqKey="Nixon R">RA Nixon</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lipton, Jo" uniqKey="Lipton J">JO Lipton</name></author><author><name sortKey="Sahin, M" uniqKey="Sahin M">M Sahin</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Switon, K" uniqKey="Switon K">K Switon</name></author><author><name sortKey="Kotulska, K" uniqKey="Kotulska K">K Kotulska</name></author><author><name sortKey="Janusz Kaminska, A" uniqKey="Janusz Kaminska A">A Janusz-Kaminska</name></author><author><name sortKey="Zmorzynska, J" uniqKey="Zmorzynska J">J Zmorzynska</name></author><author><name sortKey="Jaworski, J" uniqKey="Jaworski J">J Jaworski</name></author></analytic></biblStruct><biblStruct><analytic><author><name 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