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Title of Journal: Mol Neurobiol

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Abbravation: Molecular Neurobiology

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Springer US

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DOI

10.1016/0304-5102(89)80025-2

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ISSN

1559-1182

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Cofilin Inhibition Restores Neuronal Cell Death in

Authors: Anusha Madineni Qasim Alhadidi Zahoor A Shah
Publish Date: 2014/12/20
Volume: 53, Issue: 2, Pages: 867-878
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Abstract

Ischemia is a condition associated with decreased blood supply to the brain eventually leading to death of neurons It is associated with a diverse cascade of responses involving both degenerative and regenerative mechanisms At the cellular level the changes are initiated prominently in the neuronal cytoskeleton Cofilin a cytoskeletal actin severing protein is known to be involved in the early stages of apoptotic cell death Evidence supports its intervention in the progression of disease states like Alzheimer’s and ischemic kidney disease In the present study we have hypothesized the possible involvement of cofilin in ischemia Using PC12 cells and mouse primary cultures of cortical neurons we investigated the potential role of cofilin in ischemia in two different in vitro ischemic models chemical induced oxidative stress and oxygenglucose deprivation/reperfusion OGD/R The expression profile studies demonstrated a decrease in phosphocofilin levels in all models of ischemia implying stressinduced cofilin activation Furthermore calcineurin and slingshot 1L SSH phosphatases were found to be the signaling mediators of the cofilin activation In primary cultures of cortical neurons cofilin was found to be significantly activated after 1 h of OGD To delineate the role of activated cofilin in ischemia we knocked down cofilin by small interfering RNA siRNA technique and tested the impact of cofilin silencing on neuronal viability Cofilin siRNAtreated neurons showed a significant reduction of cofilin levels in all treatment groups control OGD and OGD/R Additionally cofilin siRNAreduced cofilin mitochondrial translocation and caspase 3 cleavage with a concomitant increase in neuronal viability These results strongly support the active role of cofilin in ischemiainduced neuronal degeneration and apoptosis We believe that targeting this protein mediator has a potential for therapeutic intervention in ischemic brain injury and strokeThe study was partly funded by a grant from NIH R00AT004197 and startup funds from The University of Toledo to ZAS Qasim Alhadidi was supported by Higher Committee for Education Development in Iraq wwwhcediraqorg The authors would like to thank Charisse N Montgomery for her assistance in the manuscript editing

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