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Author Notes:

Corresponding author: Ling Wei, MD, Department of Anesthesiology, 101 Woodruff Circle, Suite 617, Emory University School of Medicine, Atlanta, GA 30322, Tel. 404-712-8661, Fax 404-712-1351, lwei7@emory.edu

Subjects:

Research Funding:

This work was supported by NIH grants NS 37372, NS 045155, and NS 045810, and American Heart Association Established Investigator Award.

Keywords:

  • Cortical neurons
  • Apelin
  • Serum deprivation
  • Apoptosis

Neuroprotective Effect of the Endogenous Neural Peptide Apelin in Cultured Mouse Cortical Neurons

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Journal Title:

Experimental Cell Research

Volume:

Volume 316, Number 11

Publisher:

, Pages 1773-1783

Type of Work:

Article | Post-print: After Peer Review

Abstract:

The adipocytokine apelin and its G protein-coupled APJ receptor were initially isolated from a bovine stomach and have been detected in the brain and cardiovascular system. Recent studies suggest that apelin can protect cardiomyocytes from ischemic injury. Here, we investigated the effect of apelin on apoptosis in mouse primary cultures of cortical neurons. Exposure of the cortical cultures to a serum-free medium for 24 hrs induced nuclear fragmentation and apoptotic death; apelin-13 (1.0 – 5.0 nM) markedly prevented the neuronal apoptosis. Apelin neuroprotective effects were mediated by multiple mechanisms. Apelin-13 reduced serum deprivation (SD)-induced ROS generation, mitochondria depolarization, cytochrome c release and activation of caspase-3. Apelin-13 prevented SD-induced changes in phosphorylation status of Akt and ERK1/2. In addition, apelin-13 attenuated NMDA-induced intracellular Ca2+ accumulation. These results indicate that apelin is an endogenous neuroprotective adipocytokine that may block apoptosis and excitotoxic death via cellular and molecular mechanisms. It is suggested that apelins may be further explored as a potential neuroprotective reagent for ischemia-induced brain damage.

Copyright information:

© 2010 Elsevier Inc. All rights reserved.

This is an Open Access work distributed under the terms of the Creative Commons Attribution-NonCommerical-NoDerivs 3.0 Unported License (http://creativecommons.org/licenses/by-nc-nd/3.0/).

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