Prolonged translation arrest in reperfused hippocampal cornu Ammonis 1 is mediated by stress granules

Kayali, Foaz; Montie, Heather L.; Rafols, José A.; DeGracia, Donald J.

doi:10.1016/j.neuroscience.2005.05.047

Cited by 52 publications

(98 citation statements)

References 49 publications

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“…Double-labeling immunohistochemistry was performed as previously described (Kayali et al, 2005;. Pair-wise double staining of ubiquitin and TIA-1, ubiquitin and S6, and TIA-1 and S6 were performed on adjacent, 50 micron tissue sections.…”

Section: Immunohistochemistrymentioning

confidence: 99%

“…Secondary antisera dilutions were 1:300 in 1 % normal donkey serum in PBS containing 0.3% Triton X-100. Slides were examined on an Axioplan 2 Imaging System (Carl Zeiss, Oberkochen, Germany) equipped with an ApoTome, and optical sectioning was performed using the X63 oil immersion objective to generate z-stacks as previously described (Kayali et al, 2005. Fluorescent micrographs shown in the figures are orthographic projections of 3.75 micron z-stacks (15 x 0.25 micron optical sections) unless otherwise stated.…”

Section: Immunohistochemistrymentioning

confidence: 99%

“…"Yellow channels" were constructed from orthographic projections of acquired z-stacks of CA1, and colocalization, in discreet spots, of paired antigens was quantified in BioImage Intelligent Quantifier, as previously described (Kayali et al, 2005;.. Variables measured in yellow channels included spot coordinates, spot area and spot density, which were used to calculate total number of spots and total spot density. These were further normalized per the number of cells in each image for the experimental groups to give values for the "number of spots per cell" and the average "density per spot", as shown in the graphs.…”

Section: Quantitative Analysis Of Colocalizationmentioning

confidence: 99%

“…We previously described S6 and TIA-1 staining in neurons (Kayali et al, 2005). SGs have now been independently described in rat brain (Kim et al, 2006).…”

Section: Stress Granule Stainingmentioning

confidence: 99%

“…SGs are thought to sequester and protect mRNAs during periods of stress-induced translation arrest (Nover et al, 1989), and to perform functions related to cytoplasmic mRNA metabolism (Anderson and Kedersha 2006). Following global I/R, ribosomal protein S6, as a marker of the small ribosomal subunit (40S), was observed to be exclusively sequestered in SGs only in CA1 at 4 hr reperfusion following resuscitation from a 10 min cardiac arrest (Kayali et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

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Convergence of stress granules and protein aggregates in hippocampal cornu ammonis 1 at later reperfusion following global brain ischemia

et al. 2007

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The delayed and selective vulnerability of post-ischemic hippocampal CA1 pyramidal neurons correlates with a lack of recovery of normal protein synthesis. Recent evidence implicates sequestration of translational machinery into protein aggregates and stress granules as factors underlying persistent translation arrest in CA1 neurons. However, the relationship between protein aggregates and stress granules during brain reperfusion is unknown. Here we investigated the colocalization of protein aggregates and stress granules using immunofluorescence microscopy and pair-wise double labeling for ubiquitin/TIA-1, ubiquitin/small ribosomal protein S6, and TIA-1/S6. We evaluated the rat dorsal hippocampus at 1, 2 or 3 days reperfusion following a 10 min global brain ischemic insult. At 1 day reperfusion, ubiquitin-containing aggregates (ubi-protein clusters) occurred in neurons but did not colocalize with stress granules. At 2 days reperfusion, only in CA1, cytoplasmic protein aggregates colocalized with stress granules, and ubiquitin-containing inclusions accumulated in the nuclei of CA1 pyramidal neurons. Functionally, a convergence of stress granules and protein aggregates would be expected to sustain translation arrest and inhibit clearance of ubiquinated proteins, both factors expected to contribute to CA1 pyramidal neuron vulnerability.

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Section: Immunohistochemistrymentioning

confidence: 99%

Section: Immunohistochemistrymentioning

confidence: 99%

Section: Quantitative Analysis Of Colocalizationmentioning

confidence: 99%

“…We previously described S6 and TIA-1 staining in neurons (Kayali et al, 2005). SGs have now been independently described in rat brain (Kim et al, 2006).…”

Section: Stress Granule Stainingmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Convergence of stress granules and protein aggregates in hippocampal cornu ammonis 1 at later reperfusion following global brain ischemia

et al. 2007

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Structural Features of Ischemic Damage in the Hippocampus

Nikonenko

Radenović

Anđjus

et al. 2009

The Anatomical Record

118

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Cerebral ischemic injury resulting from either focal or global circulatory arrests in the brain is one of the major causes of death and disability in the adult population. The hippocampus, playing important roles in learning and memory, is selectively vulnerable to ischemic insults. Distinct populations of hippocampal neurons are targeted by ischemia and multiple factors, including excitotoxicity, oxidative stress, and inflammation, are responsible for their damage and death. Modifications of synapses occur very early after ischemia, reflecting related changes in synaptic transmission. These modifications structurally relate to spatial patterns formed by synaptic vesicles, geometry of postsynaptic density, and so forth. Ischemiainduced changes of synaptic contacts can be implicated in the mechanisms leading to delayed neuronal death. In this review, we summarize the available data on the structural aspects of ischemic injury of the hippocampus obtained in tissue culture and animal models and discuss pathways of neurodegeneration common for cerebral ischemia and various neurodegenerative disorders.

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Regulation of mRNA following brain ischemia and reperfusion

DeGracia

2017

WIREs RNA

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There is growing appreciation that mRNA regulation plays important roles in disease and injury. mRNA regulation and ribonomics occur in brain ischemia and reperfusion (I/R) following stroke and cardiac arrest and resuscitation. It was recognized over 40 years ago that translation arrest (TA) accompanies brain I/R and is now recognized as part of the intrinsic stress responses triggered in neurons. However, neuron death correlates to a prolonged TA in cells fated to undergo delayed neuronal death (DND). Dysfunction of mRNA regulatory processes in cells fated to DND prevents them from translating stress-induced mRNAs such as heat shock proteins. The morphological and biochemical studies of mRNA regulation in postischemic neurons are discussed in the context of the large variety of molecular damage induced by ischemic injury. Open issues and areas of future investigation are highlighted. A sober look at the molecular complexity of ischemia-induced neuronal injury suggests that a network framework will assist in making sense of this complexity. The ribonomic network sits between the gene network and the various protein and metabolic networks. Thus, targeting the ribonomic network may prove more effective at neuroprotection than targeting specific molecular pathways, for which all efforts have failed to the present time to stop DND in stroke and after cardiac arrest. WIREs RNA 2017, 8:e1415. doi: 10.1002/wrna.1415 For further resources related to this article, please visit the WIREs website.

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Prolonged translation arrest in reperfused hippocampal cornu Ammonis 1 is mediated by stress granules

Cited by 52 publications

References 49 publications

Convergence of stress granules and protein aggregates in hippocampal cornu ammonis 1 at later reperfusion following global brain ischemia

Convergence of stress granules and protein aggregates in hippocampal cornu ammonis 1 at later reperfusion following global brain ischemia

Structural Features of Ischemic Damage in the Hippocampus

Regulation of mRNA following brain ischemia and reperfusion

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