Abstract:
: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.
journal_name
Gliajournal_title
Gliaauthors
Hagemeier K,Lürbke A,Hucke S,Albrecht S,Preisner A,Klassen E,Hoffmann E,Cui QL,Antel J J,Brück W,Klotz L,Kuhlmann Tdoi
10.1002/glia.22552subject
Has Abstractpub_date
2013-10-01 00:00:00pages
1712-23issue
10eissn
0894-1491issn
1098-1136journal_volume
61pub_type
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