Puma, but not noxa is essential for oligodendroglial cell death.

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

Glia

journal_title

Glia

authors

Hagemeier K,Lürbke A,Hucke S,Albrecht S,Preisner A,Klassen E,Hoffmann E,Cui QL,Antel J J,Brück W,Klotz L,Kuhlmann T

doi

10.1002/glia.22552

subject

Has Abstract

pub_date

2013-10-01 00:00:00

pages

1712-23

issue

10

eissn

0894-1491

issn

1098-1136

journal_volume

61

pub_type

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