Sequential activation of necroptosis and apoptosis cooperates to mediate vascular and neural pathology in stroke.


Journal

Proceedings of the National Academy of Sciences of the United States of America
ISSN: 1091-6490
Titre abrégé: Proc Natl Acad Sci U S A
Pays: United States
ID NLM: 7505876

Informations de publication

Date de publication:
03 03 2020
Historique:
pubmed: 20 2 2020
medline: 1 7 2020
entrez: 20 2 2020
Statut: ppublish

Résumé

Apoptosis and necroptosis are two regulated cell death mechanisms; however, the interaction between these cell death pathways in vivo is unclear. Here we used cerebral ischemia/reperfusion as a model to investigate the interaction between apoptosis and necroptosis. We show that the activation of RIPK1 sequentially promotes necroptosis followed by apoptosis in a temporally specific manner. Cerebral ischemia/reperfusion insult rapidly activates necroptosis to promote cerebral hemorrhage and neuroinflammation.

Identifiants

pubmed: 32071228
pii: 1916427117
doi: 10.1073/pnas.1916427117
pmc: PMC7060720
doi:

Substances chimiques

Receptor-Interacting Protein Serine-Threonine Kinases EC 2.7.11.1
Ripk1 protein, mouse EC 2.7.11.1
Ripk3 protein, mouse EC 2.7.11.1
MAP Kinase Kinase Kinases EC 2.7.11.25
MAP kinase kinase kinase 7 EC 2.7.11.25

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

4959-4970

Subventions

Organisme : NIAID NIH HHS
ID : R01 AI075118
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA096899
Pays : United States
Organisme : NIA NIH HHS
ID : RF1 AG055521
Pays : United States
Organisme : NIA NIH HHS
ID : R21 AG059073
Pays : United States

Déclaration de conflit d'intérêts

Competing interest statement: J.Y. is a consultant of Denali Therapeutics Inc., which has licensed the necrostatin technology. M.P. received consulting and speaker fees from Genentech, GlaxoSmithKline, Boehringer Ingelheim, and Sanofi. All other authors declare no competing interests.

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Auteurs

Masanori Gomi Naito (MG)

Department of Cell Biology, Harvard Medical School, Boston, MA 02468.

Daichao Xu (D)

Department of Cell Biology, Harvard Medical School, Boston, MA 02468.

Palak Amin (P)

Department of Cell Biology, Harvard Medical School, Boston, MA 02468.

Jinwoo Lee (J)

Department of Cell Biology, Harvard Medical School, Boston, MA 02468.

Huibing Wang (H)

Department of Cell Biology, Harvard Medical School, Boston, MA 02468.

Wanjin Li (W)

Department of Cell Biology, Harvard Medical School, Boston, MA 02468.

Michelle Kelliher (M)

Department of Molecular, Cell and Cancer Biology, University of Massachusetts Medical School, Worcester, MA.

Manolis Pasparakis (M)

Institute for Genetics, University of Cologne, D-50674 Cologne, Germany.

Junying Yuan (J)

Department of Cell Biology, Harvard Medical School, Boston, MA 02468; junying_yuan@hms.harvard.edu.

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Classifications MeSH