Abstract
A worldwide epidemic of stroke is exacting a huge level of patient suffering and social
cost. The ischemia damage to neural cells and the associated permanent neural function
loss are central to the pathophysiology of stroke.
In the current study, we were endeavored to identify NR4A1, an orphan nuclear receptor
as a novel protector for neural cells in an in vitro neural ischemia model. Our results showed that oxygen and glucose deprivation (OGD)
dramatically induced primary culture neural cell apoptosis and NR4A1 expression at
both protein and mRNA level. Furthermore, hyperexpression or knock-down of NR4A1 significantly
ameliorated or exacerbated OGD induced neural damage as manifested by decreased or
increased apoptotic rates and key apoptotic protein expression respectively. As part
of effort to identify the underlying mechanism, we also found that survivin is highly
inducible following OGD and is required for NR4A1 action in this scenario.
Our data seemed to be logical extensions of previous observations showing that NR4As
are highly inducible following focal cerebral ischemia. Of note, our results also
demonstrated that NR4A1 induction in this scenario may be functionally important as
well and targeting NR4A1 protein can be intriguing as part of the effort to develop
novel therapeutic strategies for neural protection after stroke.
Keywords
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Article info
Publication history
Published online: May 09, 2013
Accepted:
April 10,
2013
Received in revised form:
April 4,
2013
Received:
December 24,
2012
Identification
Copyright
© 2013 Elsevier B.V. Published by Elsevier Inc. All rights reserved.