Mol. Cells 2017; 40(11):
Epoxyeicosatrienoic Acid Inhibits the Apoptosis of Cerebral Microvascular Smooth Muscle Cells by Oxygen Glucose Deprivation via Targeting the JNK/c-jun and MTOR Signaling Pathways
Youyang Qu, Yu Liu, Yanmei Zhu, Li Chen, Wei Sun*, and Yulan Zhu*
Department of Neurology, the Second Affiliated Hospital of Harbin Medical University, Harbin 150086, P. R. China
*Correspondence: (YZ); (WS)
Received May 19, 2017; Revised August 25, 2017; Accepted October 10, 2017.; Published online October 27, 2017.
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As a component of the neurovascular unit, cerebral smooth muscle cells (CSMCs) are an important mediator in the development of cerebral vascular diseases such as stroke. Epoxyeicosatrienoic acids (EETs) are the products of arachidonic acid catalyzed by cytochrome P450 epoxygenase. EETs are shown to exert neuroprotective effects. In this article, the role of EET in the growth and apoptosis of CSMCs and the underlying mechanisms under oxygen glucose deprivation (OGD) conditions were addressed. The viability of CMSCs was decreased significantly in the OGD group, while different subtypes of EETs, especially 14,15-EET, could increase the viability of CSMCs under OGD conditions. RAPA (serine/threonine kinase Mammalian Target of Rapamycin), a specific mTOR inhibitor, could elevate the level of oxygen free radicals in CSMCs as well as the anti-apoptotic effects of 14,15-EET under OGD conditions. However, SP600125, a specific JNK (c-Jun Nterminal protein kinase) pathway inhibitor, could attenuate oxygen free radicals levels in CSMCs as well as the antiapoptotic effects of 14,15-EET under OGD conditions. These results strongly suggest that EETs exert protective functions during the growth and apoptosis of CSMCs, via the JNK/c-jun and mTOR signaling pathways in vitro. We are the first to disclose the beneficial roles and underlying mechanism of 14,15-EET in CSMC under OGD conditions.
Keywords: cerebral ischemia/reperfusion injury, epoxyeicosatrienoic acids, JNK/c-jun pathway, mTOR pathway

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31 October 2017 Volume 40,
Number 10, pp. 697~804

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