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Volume 8, Issue 6
J Neurol Neurosci
ISSN: 2171-6625 Neuro, an open access journal
Neuroscience 2017
October 16-17, 2017
Page 14
Notes:
conference
series
.com
OCTOBER 16-17, 2017 OSAKA, JAPAN
17
TH
Global Neuroscience Conference
PKCε-ATF2 signaling in ischemia-induced neurodegeneration
C
ardiac arrest continues to be the leading cause of death worldwide. Global cerebral ischemia that accompanies cardiac
arrest is one of the major causes of morbidity and mortality. Out of many therapeutic approaches investigated, one of them
is ischemic preconditioning, which is sufficient to protect brain tissues from subsequent lethal ischemic insult. PKCε peptide
activator administered before, but not after, ischemia mediates preconditioning and confers neuro protection. However, the
use of preconditioning as a therapeutic approach has not become standard clinical practice because the occurrence of cardiac
arrest and cerebral ischemia is sudden and unpredictable. Thus, post-ischemic therapeutic targets have to be unraveled. The
beneficial effects of PKCε peptide activators in ischemic preconditioning stimulate interests in understanding the molecular
and cellular actions of PKCε after global cerebral ischemia. A detailed understanding of PKCε signaling pathways requires
identification of its downstream targets.This study is to determine the downstreammediators of PKCε, so that novel therapeutic
targets can be developed. We found that PKCε mediated the phosphorylation of Activating Transcription Factor 2 (ATF2)
at threonine 52 in the hippocampus. ATF2 is a member of the Activator Protein 1 (AP1) transcription factor superfamily
regulating normal growth and development as well as response to cellular stress. In response to global cerebral ischemia, PKCε
expression was gradually decreased. This resulted in leakage of nuclear ATF2 to the mitochondria and subsequent ischemia-
induced neurodegeneration. This study not only provides the first insight into the neuronal cell death regulated by PKCε and
ATF2, but also establishes a strong base to develop new classes of therapeutic molecules to inhibit the leakage of ATF2 and
reduce brain injury after cardiac arrest.
Biography
Wen-Hai Chou has completed his PhD from Department of Molecular Medicine, University of Texas Health Science Center, San Antonio and Post-Doctoral studies
from University of California, San Francisco. He is an Assistant Investigator of National Health Research Institutes, Taiwan. He has published more than 22 papers
in reputed journals including
Neuron, Journal of Clinical Investigation, Journal of Neuroscience
and
Journal of Biological Chemistry
.
wenhaichou@nhri.org.twWen-Hai Chou
National Health Research Institutes, Taiwan
Wen-Hai Chou, J Neurol Neurosci 2017, 8:6
DOI: 10.21767/2171-6625-C1-004