当前位置: 首页 > 详情页

ESM-1 promotes adhesion between monocytes and endothelial cells under intermittent hypoxia

文献详情

资源类型:

收录情况: ◇ SCIE

机构: [1]Department of Otolaryngology, Beijing Anzhen Hospital, Capital Medical University, Beijing, China [2]The Key Laboratory of Upper Airway Dysfunction‐Related Cardiovascular Diseases, Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing Anzhen Hospital, Capital Medical University, Beijing, China
出处:
ISSN:

关键词: adhesion endothelial dysfunction endothelial-cell-specific molecule-1 (ESM-1) intermittent hypoxia (IH)

摘要:
Intermittent hypoxia (IH), the key property of obstructive sleep apnea (OSA), is closely associated with endothelial dysfunction. Endothelial-cell-specific molecule-1 (ESM-1, Endocan) is a novel, reported molecule linked to endothelial dysfunction. The aim of this study is to evaluate the effect of IH on ESM-1 expression and the role of ESM-1 in endothelial dysfunction. We found that serum concentration of ESM-1, inter-cellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) is significantly higher in patients with OSA than healthy volunteers (p < 0.01). The expression of ESM-1, hypoxia-inducible factor-1 alpha (HIF-1 alpha), and vascular endothelial growth factor (VEGF) was significantly increased in human umbilical vein endothelial cells (HUVECs) by treated IH in a time-dependent manner. HIF-1 alpha short hairpin RNA and vascular endothelial growth factor receptor (VEGFR) inhibitor inhibited the expression of ESM-1 in HUVECs. ICAM-1 and VCAM-1 expressions were significantly enhanced under IH status, accompanied by increased monocyte-endothelial cell adhesion rate (p < 0.001). Accordingly, ESM-1 silencing decreased the expression of ICAM-1 and VCAM-1 in HUVECs, whereas ESM-1 treatment significantly enhanced ICAM-1 expression accompanied by increasing adhesion ability. ESM-1 is significantly upregulated by the HIF-1 alpha/VEGF pathway under IH in endothelial cells, playing a critical role in enhancing adhesion between monocytes and endothelial cells, which might be a potential target for IH-induced endothelial dysfunction.

基金:
语种:
被引次数:
WOS:
PubmedID:
中科院(CAS)分区:
出版当年[2018]版:
大类 | 2 区 生物
小类 | 2 区 生理学 3 区 细胞生物学
最新[2023]版:
大类 | 2 区 生物学
小类 | 2 区 生理学 3 区 细胞生物学
JCR分区:
出版当年[2017]版:
Q1 PHYSIOLOGY Q2 CELL BIOLOGY
最新[2023]版:
Q1 PHYSIOLOGY Q2 CELL BIOLOGY

影响因子: 最新[2023版] 最新五年平均 出版当年[2017版] 出版当年五年平均 出版前一年[2016版] 出版后一年[2018版]

第一作者:
第一作者机构: [1]Department of Otolaryngology, Beijing Anzhen Hospital, Capital Medical University, Beijing, China
通讯作者:
通讯机构: [1]Department of Otolaryngology, Beijing Anzhen Hospital, Capital Medical University, Beijing, China [2]The Key Laboratory of Upper Airway Dysfunction‐Related Cardiovascular Diseases, Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing Anzhen Hospital, Capital Medical University, Beijing, China [*1]Department of Otolaryngology, Beijing Anzhen Hospital, Capital Medical University, No. 2 Anzhen Road, Beijing 100029, China.
推荐引用方式(GB/T 7714):
APA:
MLA:

资源点击量:16409 今日访问量:0 总访问量:869 更新日期:2025-01-01 建议使用谷歌、火狐浏览器 常见问题

版权所有©2020 首都医科大学宣武医院 技术支持:重庆聚合科技有限公司 地址:北京市西城区长椿街45号宣武医院