Apelin-13 upregulates Egr-1 expression in rat vascular smooth muscle cells through the PI3K/Akt and PKC signaling pathways

被引:17
作者
Liu, Qi-Feng [1 ]
Yu, Hong-Wei [2 ]
Sun, Li-Li [3 ]
You, Lu [1 ]
Tao, Gui-Zhou [1 ]
Qu, Bao-Ze [1 ]
机构
[1] Liaoning Med Univ, Affiliated Hosp 1, Dept Cardiol, Jinzhou 121001, Liaoning, Peoples R China
[2] Jinzhou Cent Hosp, Dept Cardiol, Jinzhou 121001, Peoples R China
[3] Liaoning Med Univ, Affiliated Hosp 3, Dept Ophthalmol, Jinzhou 121001, Liaoning, Peoples R China
关键词
Signal transduction; G protein; MAPK; PKC; PI3K/Akt; Egr-1; ISCHEMIA/REPERFUSION INJURY; TRANSDUCTION PATHWAY; GROWTH-FACTOR; PROLIFERATION; MIGRATION; ATHEROSCLEROSIS; ERK1/2; APELIN/APJ; AKT;
D O I
10.1016/j.bbrc.2015.10.171
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Previous studies have shown that Apelin-13 upregulates early growth response factor-1 (Egr-1) via the extracellular signal-regulated protein kinase (ERK) signaling pathway. Apelin-13 induces proliferation and migration of vascular smooth muscle cells (VSMCs) as well as the upregulation of osteopontin (OPN) via the upregulation of Egr-1. This study was designed to further explore the activity of Apelin-13 in VSMCs by investigating members of the mitogen-activated protein kinase (MAPK) family, in particular Jun kinase (JNK) and p38 mitogen-activated protein kinase (P38). We also examined whether the phosphatidylinositol 3 kinase (PI3K)/protein kinase B (Ala) and protein kinase C (PKC) signaling pathways were involved in the regulation of Egr-1 by Apelin-13. We treated rat aortic VSMCs with Apelin-13 and examined the expression of JNK, p-JNK, P38, and p-P38 to investigate whether Apelin-13-mediated increases in Egr-1 occurred through the JNK and P38 signaling pathways. We then pretreated VSMCs with the Gi protein inhibitor pertussis toxin (PTX) and the Gq inhibitor YM254890, added Apelin-13 and looked for changes in Egr-1 expression. Finally, we pretreated with the PI3K inhibitor LY294002 and the PKC inhibitor GF109203X, and treated with Apelin-13. Our results showed that JNK and P38 did not participate in Apelin-13-mediated increase in Egr-1. Instead, Apelin-13 upregulation of Egr-1 was mediated by a PTX-sensitive Gi protein. Apelin-13 did increase ERK phosphorylation through the PI3K/Akt and PKC signaling pathways, resulting in changes in Egr-1 expression. These data provide important targets for future studies to modulate vascular remodeling. (C) 2015 Elsevier Inc. All rights reserved.
引用
收藏
页码:617 / 621
页数:5
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