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Bai, X.* ; Zhao, N.* ; Koupourtidou; C. ; Fang, L.P.* ; Schwarz, V. ; Caudal, L.C.* ; Zhao, R.* ; Hirrlinger, J.* ; Walz, W.* ; Bian, S.* ; Huang, W.* ; Ninkovic, J. ; Kirchhoff, F.* ; Scheller, A.*

In the mouse cortex, oligodendrocytes regain a plastic capacity, transforming into astrocytes after acute injury.

Dev. Cell 58, 1153-1169.e5 (2023)
DOI PMC
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Acute brain injuries evoke various response cascades directing the formation of the glial scar. Here, we report that acute lesions associated with hemorrhagic injuries trigger a re-programming of oligodendrocytes. Single-cell RNA sequencing highlighted a subpopulation of oligodendrocytes activating astroglial genes after acute brain injuries. By using PLP-DsRed1/GFAP-EGFP and PLP-EGFPmem/GFAP-mRFP1 transgenic mice, we visualized this population of oligodendrocytes that we termed AO cells based on their concomitant activity of astro- and oligodendroglial genes. By fate mapping using PLP- and GFAP-split Cre complementation and repeated chronic in vivo imaging with two-photon laser-scanning microscopy, we observed the conversion of oligodendrocytes into astrocytes via the AO cell stage. Such conversion was promoted by local injection of IL-6 and was diminished by IL-6 receptor-neutralizing antibody as well as by inhibiting microglial activation with minocycline. In summary, our findings highlight the plastic potential of oligodendrocytes in acute brain trauma due to microglia-derived IL-6.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Il-6 ; Acute Brain Injury ; Astrocyte ; Differentiation ; Fate Switch ; Oligodendrocyte; Fibrillary Acidic Protein; Cell Fate Determination; Central-nervous-system; Ng2 Glia; Progenitor Cells; Nmda Receptors; White-matter; Stem-cells; Differentiation; Lineage
ISSN (print) / ISBN 1534-5807
e-ISSN 1878-1551
Zeitschrift Developmental Cell
Quellenangaben Band: 58, Heft: 13, Seiten: 1153-1169.e5 Artikelnummer: , Supplement: ,
Verlag Elsevier
Verlagsort 50 Hampshire St, Floor 5, Cambridge, Ma 02139 Usa
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Förderungen
University of Saarland
European Commission
BMBF (EraNet-Neuron BrIE)
Deutsche Forschungsgemeinschaft