Puma, but not noxa is essential for oligodendroglial cell death. Issue 10 (6th August 2013)

• Record Type: Journal Article
• Authors: Hagemeier, Karin; Lürbke, Alexander; Hucke, Stephanie; Albrecht, Stefanie; Preisner, Anna; Klassen, Elena; Hoffmann, Elke; Cui, Qiao‐Ling; Antel J, Jack; Brück, Wolfgang; Klotz, Luisa; Kuhlmann, Tanja
• Is Part Of: Glia. Volume 61:Issue 10(2013:Oct.)
• Page Start: 1712
• Page End: 1723
• Publication Date: 2013-08-06
• Subjects: demyelinating diseases -- cuprizone model -- apoptosis -- BH3 only protein; Neuroglia -- Periodicals; Neurology -- Periodicals; 611.0188
• DOI: 10.1002/glia.22552
• Languages: English
• ISSNs: 0894-1491

Abstract

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. GLIA 2013;61:1712–1723