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; Yulan Zhu

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자료유형: 학술저널

저자정보: Youyang Qu (the Second Affiliated Hospital of Harbin Medical University) Yu Liu (the Second Affiliated Hospital of Harbin Medical University) Yanmei Zhu (the Second Affiliated Hospital of Harbin Medical University) Li Chen (the Second Affiliated Hospital of Harbin Medical University) Wei Sun (the Second Affiliated Hospital of Harbin Medical University) Yulan Zhu (the Second Affiliated Hospital of Harbin Medical University)

저널정보: 한국분자세포생물학회 Molecules and Cells Molecules and Cells 제40권 제11호

발행연도: 2017.11

수록면: 837 - 846 (10page)

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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. Epoxye-icosatrienoic acids (EETs) are the products of ara-chidonic 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 N-terminal protein kinase) pathway inhibitor, could attenuate oxygen free radicals levels in CSMCs as well as the anti-apoptotic 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.

#cerebral ischemia/reperfusion injury #epoxyeicosatrienoic acids #JNK/c-Jun pathway #mTOR pathway

참고문헌 (43)

참고문헌 신청

Abbott, N. J. / 2006 / Astrocyteendothelial interactions at the blood-brain barrier / Nat. Rev. Neurosci 7:41~53

Benoit, M. / 2011 / Targeting the JNK signaling pathway potentiates the antiproliferative efficacy of rapamycin in LS174T colon cancer cells / J. Surg. Res 167:e193~e198

Brakemeier, S. / 2003 / Shear stress-induced upregulation of the intermediate-conductance Ca(2+)-activated K(+)channel in human endothelium / Cardiov. Res 60:488~496

Briones, A. M. / 2010 / Oxidative stress and hypertension: current concepts / Curr. Hypertension Rep 12:135~142

Brooks, C. / 2007 / Regulation of mitochondrial morphological dynamics during apoptosis by Bcl-2 family proteins: a key in Bak? / Cell Cycle 6:3043~3047

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