Gastrin-releasing peptide induces monocyte adhesion to vascular endothelium by upregulating endothelial adhesion molecules
Gastrin-releasing peptide induces monocyte adhesion to vascular endothelium by upregulating endothelial adhesion molecules
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DOI：
10.1016/j.bbrc.2017.01.058
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发表时间：
2017-04-01
影响因子：
3.1
通讯作者：
Bae, Moon-Kyoung
中科院分区：
文献类型：
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作者：
Kim, Mi-Kyoung;Park, Hyun-Joo;Bae, Moon-Kyoung
胃泌素释放肽（GRP）是一种神经肽，在包括外周组织炎症性疾病在内的多种病理生理条件下发挥作用，但GRP是否能直接调节内皮炎症过程尚不清楚。在这项研究中，我们表明，GRP促进白细胞粘附到人脐静脉内皮细胞（HUVECs）和主动脉内皮细胞。GRP可通过激活内皮细胞核因子-κ B（NF-κ B）增加细胞间粘附分子-1（ICAM-1）和血管细胞粘附分子-1（VCAM-1）的表达。此外，GRP激活细胞外信号调节激酶1/2（ERK 1/2），p38 MAPK和AKT，这些信号通路的抑制显着减少GRP诱导的单核细胞粘附到内皮细胞。总的来说，我们的研究结果表明，GRP可能会导致内皮功能障碍，这可能是特别相关的血管炎症性疾病的发展。(C)2017爱思唯尔公司All rights reserved.
Gastrin-releasing peptide (GRP) is a neuropeptide that plays roles in various pathophysiological conditions including inflammatory diseases in peripheral tissues; however, little is known about whether GRP can directly regulate endothelial inflammatory processes. In this study, we showed that GRP promotes the adhesion of leukocytes to human umbilical vein endothelial cells (HUVECs) and the aortic endothelium. GRP increased the expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) by activating nuclear factor-KB (NF-KB) in endothelial cells. In addition, GRP activated extracellular signal-regulated kinase 1/2 (ERK1/2), p38MAPK, and AKT, and the inhibition of these signaling pathways significantly reduced GRP-induced monocyte adhesion to the endothelium. Overall, our results suggested that GRP may cause endothelial dysfunction, which could be of particular relevance in the development of vascular inflammatory disorders.(C) 2017 Elsevier Inc. All rights reserved.