Journal
BRAIN RESEARCH
Volume 1668, Issue -, Pages 1-11Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.brainres.2017.05.009
Keywords
Transglutaminase 2; Ischemia; NF-kappa B; Astrocyte; Viability; p38; JNK; ERK1/2; Transamidation; Oxygen/glucose deprivation
Categories
Funding
- National Institutes of Health [R01 NS065825, F31 NS081894]
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Transglutaminase 2 (TG2) is a multifunctional protein that can contribute to cell death and cell survival processes in a variety of disease contexts. Within the brain, TG2 has been shown to promote cell death in ischemic injury when expressed in astrocytes (Colak and Johnson, 2012). However, the specific functions and characteristics of astrocytic TG2 that mediate this effect are largely unknown. Therefore, the goal of this study was to investigate the role of astrocytic TG2 in mediating cellular viability processes in the context of ischemic injury, with a specific focus on its contributions to intracellular signaling cascades. We show that, in response to oxygen glucose deprivation (OGD), acute lentiviral-mediated knockdown of TG2, as well as inhibition with an irreversible TG2 inhibitor, enhances cell survival. We also show that TG2 depletion increases nuclear factor-kappa B (NF-kappa B) signaling, whereas inhibition reduces NF-kappa B activity. Despite its clear contribution to NF-kappa B signaling, however, TG2 modulation of NF-kappa B signaling is not likely to be a major contributor to its ability to mediate astrocytic viability in this context. Overall, the results of this study provide insight into the role of TG2 in astrocytes and suggest possible avenues for future study of the relationship between astrocytic TG2 and ischemic injury. (C) 2017 Elsevier B.V. All rights reserved.
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