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Puma, but not noxa is essential for oligodendroglial cell death
Author(s) -
Hagemeier Karin,
Lürbke Alexander,
Hucke Stephanie,
Albrecht Stefanie,
Preisner Anna,
Klassen Elena,
Hoffmann Elke,
Cui QiaoLing,
Antel J Jack,
Brück Wolfgang,
Klotz Luisa,
Kuhlmann Tanja
Publication year - 2013
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.22552
Subject(s) - puma , programmed cell death , biology , staurosporine , oligodendrocyte , apoptosis , microbiology and biotechnology , neuroscience , immunology , central nervous system , signal transduction , myelin , protein kinase c , genetics
The mechanisms involved in oligodendroglial cell death in human demyelinating diseases are only partly understood. Here, we demonstrate that the BH3 only protein Puma, but not Noxa, is essential for oligodendroglial cell death in toxic demyelination induced by the copper chelator cuprizone. Primary oligodendrocytes derived from Noxa‐ or Puma‐ deficient mice showed comparable differentiation to wild‐type cells, but Puma‐ deficient oligodendrocytes were less susceptible to spontaneous, staurosporine, or nitric oxide‐induced cell death. Furthermore, Puma was expressed in oligodendrocytes in multiple sclerosis (MS) lesions and Puma mRNA levels were upregulated in primary human oligodendrocytes upon cell death induction by staurosporine. Our data demonstrate that Puma is pivotal for oligodendroglial cell death induced by different cell death stimuli and might play a role in oligodendroglial cell death in MS. GLIA 2013;61:1712–1723