miR-218 Inhibits Mitochondrial Clearance by Targeting PRKN E3 Ubiquitin Ligase
Identifieur interne : 000007 ( an2020/Analysis ); précédent : 000006; suivant : 000008miR-218 Inhibits Mitochondrial Clearance by Targeting PRKN E3 Ubiquitin Ligase
Auteurs : Anthea Di Rita [Italie] ; Teresa Maiorino ; Krenare Bruqi [Italie] ; Floriana Volpicelli [Italie] ; Gian Carlo Bellenchi [Italie] ; Flavie StrappazzonSource :
- International Journal of Molecular Sciences [ 1422-0067 ] ; 2020.
Abstract
The selective elimination of dysfunctional mitochondria through mitophagy is crucial for preserving mitochondrial quality and cellular homeostasis. The most described mitophagy pathway is regulated by a positive ubiquitylation feedback loop in which the PINK1 (PTEN induced kinase 1) kinase phosphorylates both ubiquitin and the E3 ubiquitin ligase PRKN (Parkin RBR E3 ubiquitin ligase), also known as PARKIN. This event recruits PRKN to the mitochondria, thus amplifying ubiquitylation signal. Here we report that miR-218 targets PRKN and negatively regulates PINK1/PRKN-mediated mitophagy. Overexpression of miR-218 reduces PRKN mRNA levels, thus also reducing protein content and deregulating the E3 ubiquitin ligase action. In fact, following miR-218 overexpression, mitochondria result less ubiquitylated and the autophagy machinery fails to proceed with correct mitochondrial clearance. Since mitophagy defects are associated with various human diseases, these results qualify miR-218 as a promising therapeutic target for human diseases.
Url:
DOI: 10.3390/ijms21010355
PubMed: 31948106
PubMed Central: 6981953
Affiliations:
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PMC:6981953Le document en format XML
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Santa Lucia, 00143 Rome, Italy;<email>antheadirita@gmail.com</email> (A.D.R.);<email>maiorino.teresa@gmail.com</email> (T.M.);<email>krenare.bruqi@gmail.com</email> (K.B.);<email>bellenchi@igb.cnr.it</email> (G.C.B.)</nlm:aff></affiliation><affiliation wicri:level="1"><nlm:aff id="af2-ijms-21-00355">University of Rome Tor Vergata, 00133 Rome, Italy</nlm:aff><country xml:lang="fr">Italie</country><wicri:regionArea>University of Rome Tor Vergata, 00133 Rome</wicri:regionArea><placeName><settlement type="city">Rome</settlement><region nuts="2">Latium</region></placeName></affiliation></author><author><name sortKey="Maiorino, Teresa" sort="Maiorino, Teresa" uniqKey="Maiorino T" first="Teresa" last="Maiorino">Teresa Maiorino</name><affiliation><nlm:aff id="af1-ijms-21-00355">IRCCS Fondazione Santa Lucia, 00143 Rome, Italy;<email>antheadirita@gmail.com</email> (A.D.R.);<email>maiorino.teresa@gmail.com</email> (T.M.);<email>krenare.bruqi@gmail.com</email> 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last="Volpicelli">Floriana Volpicelli</name><affiliation><nlm:aff id="af3-ijms-21-00355">Institute of Genetics and Biophysics “Adriano Buzzati Traverso”, CNR, 80131 Naples, Italy;<email>floriana.volpicelli@unina.it</email></nlm:aff></affiliation><affiliation wicri:level="1"><nlm:aff id="af4-ijms-21-00355">Department of Pharmacy, University of Naples Federico II, 80131 Naples, Italy</nlm:aff><country xml:lang="fr">Italie</country><wicri:regionArea>Department of Pharmacy, University of Naples Federico II, 80131 Naples</wicri:regionArea><wicri:noRegion>80131 Naples</wicri:noRegion></affiliation></author><author><name sortKey="Bellenchi, Gian Carlo" sort="Bellenchi, Gian Carlo" uniqKey="Bellenchi G" first="Gian Carlo" last="Bellenchi">Gian Carlo Bellenchi</name><affiliation><nlm:aff id="af1-ijms-21-00355">IRCCS Fondazione Santa Lucia, 00143 Rome, Italy;<email>antheadirita@gmail.com</email> (A.D.R.);<email>maiorino.teresa@gmail.com</email> (T.M.);<email>krenare.bruqi@gmail.com</email> (K.B.);<email>bellenchi@igb.cnr.it</email> (G.C.B.)</nlm:aff></affiliation><affiliation><nlm:aff id="af3-ijms-21-00355">Institute of Genetics and Biophysics “Adriano Buzzati Traverso”, CNR, 80131 Naples, Italy;<email>floriana.volpicelli@unina.it</email></nlm:aff></affiliation><affiliation wicri:level="1"><nlm:aff id="af5-ijms-21-00355">Department of Systems Medicine, University of Rome Tor Vergata, 00133 Rome, Italy</nlm:aff><country xml:lang="fr">Italie</country><wicri:regionArea>Department of Systems Medicine, University of Rome Tor Vergata, 00133 Rome</wicri:regionArea><placeName><settlement type="city">Rome</settlement><region nuts="2">Latium</region></placeName></affiliation></author><author><name sortKey="Strappazzon, Flavie" sort="Strappazzon, Flavie" uniqKey="Strappazzon F" first="Flavie" last="Strappazzon">Flavie Strappazzon</name><affiliation><nlm:aff id="af1-ijms-21-00355">IRCCS Fondazione Santa Lucia, 00143 Rome, Italy;<email>antheadirita@gmail.com</email> (A.D.R.);<email>maiorino.teresa@gmail.com</email> (T.M.);<email>krenare.bruqi@gmail.com</email> (K.B.);<email>bellenchi@igb.cnr.it</email> (G.C.B.)</nlm:aff></affiliation></author></analytic><series><title level="j">International Journal of Molecular Sciences</title><idno type="eISSN">1422-0067</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>The selective elimination of dysfunctional mitochondria through mitophagy is crucial for preserving mitochondrial quality and cellular homeostasis. The most described mitophagy pathway is regulated by a positive ubiquitylation feedback loop in which the PINK1 (PTEN induced kinase 1) kinase phosphorylates both ubiquitin and the E3 ubiquitin ligase PRKN (Parkin RBR E3 ubiquitin ligase), also known as PARKIN. This event recruits PRKN to the mitochondria, thus amplifying ubiquitylation signal. Here we report that miR-218 targets PRKN and negatively regulates PINK1/PRKN-mediated mitophagy. Overexpression of miR-218 reduces PRKN mRNA levels, thus also reducing protein content and deregulating the E3 ubiquitin ligase action. In fact, following miR-218 overexpression, mitochondria result less ubiquitylated and the autophagy machinery fails to proceed with correct mitochondrial clearance. Since mitophagy defects are associated with various human diseases, these results qualify miR-218 as a promising therapeutic target for human diseases.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Cecconi, F" uniqKey="Cecconi F">F. Cecconi</name></author><author><name sortKey="Levine, B" uniqKey="Levine B">B. Levine</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lemasters, J J" uniqKey="Lemasters J">J.J. Lemasters</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Tatsuta, T" uniqKey="Tatsuta T">T. Tatsuta</name></author><author><name sortKey="Langer, T" uniqKey="Langer T">T. Langer</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Wang, D D" uniqKey="Wang D">D.D. Wang</name></author><author><name sortKey="Jin, M F" uniqKey="Jin M">M.F. Jin</name></author><author><name sortKey="Zhao, D J" uniqKey="Zhao D">D.J. 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Cordelières</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>Italie</li></country><region><li>Latium</li></region><settlement><li>Rome</li></settlement></list><tree><noCountry><name sortKey="Maiorino, Teresa" sort="Maiorino, Teresa" uniqKey="Maiorino T" first="Teresa" last="Maiorino">Teresa Maiorino</name><name sortKey="Strappazzon, Flavie" sort="Strappazzon, Flavie" uniqKey="Strappazzon F" first="Flavie" last="Strappazzon">Flavie Strappazzon</name></noCountry><country name="Italie"><region name="Latium"><name sortKey="Di Rita, Anthea" sort="Di Rita, Anthea" uniqKey="Di Rita A" first="Anthea" last="Di Rita">Anthea Di Rita</name></region><name sortKey="Bellenchi, Gian Carlo" sort="Bellenchi, Gian Carlo" uniqKey="Bellenchi G" first="Gian Carlo" last="Bellenchi">Gian Carlo Bellenchi</name><name sortKey="Bruqi, Krenare" sort="Bruqi, Krenare" uniqKey="Bruqi K" first="Krenare" last="Bruqi">Krenare Bruqi</name><name sortKey="Volpicelli, Floriana" sort="Volpicelli, Floriana" uniqKey="Volpicelli F" first="Floriana" last="Volpicelli">Floriana Volpicelli</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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