Role of the epigenetic factor Sirt7 in neuroinflammation and neurogenesis. (June 2018)

• Record Type: Journal Article
• Authors: Burg, Nicolas; Bittner, Stefan; Ellwardt, Erik
• Is Part Of: Neuroscience research. Volume 131(2018)
• Page Start: 1
• Page End: 9
• Publication Date: 2018-06
• Subjects: Sirt7 -- EAE -- Epigenetic -- Multiple sclerosis -- Neuroinflammation -- Adult neurogenesis; Neurosciences -- Research -- Periodicals; Neurosciences -- Research -- Japan -- Periodicals; Neurology -- Periodicals; Neurosciences -- Periodicals; Neurosciences -- Recherche -- Périodiques; Neurosciences -- Recherche -- Japon -- Périodiques; Neurosciences -- Research; Japan; Periodicals; 612.8
• DOI: 10.1016/j.neures.2017.09.005
• Languages: English
• ISSNs: 0168-0102

Abstract

Highlights: Sirt7 modulates the adaptive immune response in EAE. Sirt7 does not influence the EAE disease course. Sirt7 favors survival of adult born neurons in the hippocampus. We find decreased hippocampal proliferation in EAE animals. Abstract: Epigenetic regulators are increasingly recognized as relevant modulators in the immune and nervous system. The class of sirtuins consists of NAD + -dependent histone deacetylases that regulate transcription. Sirtuin family member Sirt1 has already been shown to influence the disease course in an animal model of autoimmune neuroinflammation (experimental autoimmune encephalomyelitis (EAE). A role of Sirt7, a related epigenetic regulator, on immune system regulation has been proposed before, as these mice are more susceptible to develop inflammatory cardiomyopathy. Sirt7 −/− animals showed no differences in clinical score compared to wild-type littermates after EAE induction with myelin oligodendrocyte glycoprotein (MOG) peptide35-55, although we found subtle immune alterations at different phases of EAE and decreased survival of newly generated neurons in the hippocampus. Our data indicate that Sirt7 has a slight protective impact on both the adaptive immune system and neurogenesis. However, overall this epigenetic factor is not capable of impacting the acute or chronic phase of neuroinflammation.