Authors: Jamison, Jill T; Lewis, Monique K; Kreipke, Christian W; Rafols, José A; DeGracia, Donald J

Source: Neurological Research, Volume 33, Number 2, March 2011 , pp. 145-161(17)

Publisher: Maney Publishing

Abstract:

Objectives: Most work on ischemia?induced neuronal death has revolved around the relative contributions of necrosis and apoptosis, but this work has not accounted for the role of ischemia?induced stress responses. An expanded view recognizes a competition between ischemia?induced damage mechanisms and stress responses in the genesis of ischemia?induced neuronal death. An important marker of post?ischemic stress responses is inhibition of neuronal protein synthesis, a morphological correlate of which is the compartmentalization of mRNA away from ribosomes in the form of cytoplasmic mRNA granules.

Methods: Here we assessed the generality of this mRNA granule response following either 10 or 15 minutes of global brain ischemia and 1 hour of reperfusion, 4 hours of focal cerebral ischemia alone, and endothelin?1 intraventricular injection.

Results: Both global and focal ischemia led to prominent neuronal cytoplasmic mRNA granule formation in layer II cortical neurons. In addition, we report here new post?ischemic cellular phenotypes characterized by the loss of nuclear polyadenylated mRNA staining in cortical neurons following endothelin?1 treatment and 15 minutes of global ischemia. Both mRNA granulation and loss of nuclear mRNAs occurred in non?shrunken post?ischemic neurons.

Discussion: Where cytoplasmic mRNA granules generally appear to mark a protective response in surviving cells, loss of nuclear mRNAs may mark cellular damage leading to cell atrophy/death. Hence, staining for total mRNA may reveal facets of the competition between stress responses and damage mechanisms at early stages in post?ischemic neurons.

Keywords: Brain ischemia and reperfusion; Endothelin?1; mRNA granules; Protein synthesis inhibition

Document Type: Original Article

DOI: http://dx.doi.org/10.1179/016164111X12881719352255

Affiliations: Department of Physiology, Wayne State University School of Medicine, Detroit, MI, USA

Publication date: 2011-03-01

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