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Gascón, S. ; Murenu, E. ; Masserdotti, G. ; Ortega, F.* ; Russo, G.L. ; Petrik, D. ; Deshpande, A.* ; Heinrich, C.* ; Karow, M.* ; Robertson, S.P.* ; Schroeder, T. ; Beckers, J. ; Irmler, M. ; Berndt, C.* ; Friedmann Angeli, J.P.F. ; Conrad, M. ; Berninger, B.* ; Götz, M.

Identification and successful negotiation of a metabolic checkpoint in direct neuronal repogramming.

Cell Stem Cell 18, 396-409 (2016)
Verlagsversion DOI PMC
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Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Despite the widespread interest in direct neuronal reprogramming, the mechanisms underpinning fate conversion remain largely unknown. Our study revealed a critical time point after which cells either successfully convert into neurons or succumb to cell death. Co-transduction with Bcl-2 greatly improved negotiation of this critical point by faster neuronal differentiation. Surprisingly, mutants with reduced or no affinity for Bax demonstrated that Bcl-2 exerts this effect by an apoptosis-independent mechanism. Consistent with a caspase-independent role, ferroptosis inhibitors potently increased neuronal reprogramming by inhibiting lipid peroxidation occurring during fate conversion. Genome-wide expression analysis confirmed that treatments promoting neuronal reprogramming elicit an anti-oxidative stress response. Importantly, co-expression of Bcl-2 and anti-oxidative treatments leads to an unprecedented improvement in glial-to-neuron conversion after traumatic brain injury in vivo, underscoring the relevance of these pathways in cellular reprograming irrespective of cell type in vitro and in vivo.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Nonapoptotic Cell-death; Oxidative Stress; In-vivo; Brain-injury; Vitamin-d; Mitochondrial Metabolism; Lipid-peroxidation; Functional-neurons; Direct Conversion; Progenitor Cells
Sprache englisch
Veröffentlichungsjahr 2016
Prepublished im Jahr 2015
HGF-Berichtsjahr 2015
ISSN (print) / ISBN 1934-5909
e-ISSN 1875-9777
Zeitschrift Cell Stem Cell
Quellenangaben Band: 18, Heft: 3, Seiten: 396-409 Artikelnummer: , Supplement: ,
Verlag Cell Press
Verlagsort Cambridge, Mass.
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Stem Cell Research (ISF)
Institute of Experimental Genetics (IEG)
Institute of Developmental Genetics (IDG)
POF Topic(s) 30204 - Cell Programming and Repair
30201 - Metabolic Health
30502 - Diabetes: Pathophysiology, Prevention and Therapy
30504 - Mechanisms of Genetic and Environmental Influences on Health and Disease
Forschungsfeld(er) Stem Cell and Neuroscience
Genetics and Epidemiology
PSP-Element(e) G-500800-001
G-500600-004
G-500600-005
G-500600-006
G-500500-004
DOI 10.1016/j.stem.2015.12.003
WOS ID WOS:000372322200015
Scopus ID 84960106732
PubMed ID 26748418
Erfassungsdatum 2015-12-31
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