机构:[1]Department of Otolaryngology, Beijing Anzhen Hospital, Capital Medical University, Beijing, China临床科室耳鼻咽喉头颈外科首都医科大学附属安贞医院[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首都医科大学附属安贞医院
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:
Beijing Municipal Administration of Hospitals Ascent Plan [DFL20150602]; Beijing Municipal Administration of Hospitals Clinical Medicine Development of Special Funding Support [ZYLX201605]; Beijing Medical Project [2016-4]; Beijing Key Laboratory of Upper Airway Dysfunction and Related Cardiovascular Diseases [BZ0377]; National Natural Science Foundation of ChinaNational Natural Science Foundation of China [81470567]
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):
Haili Sun,Huina Zhang,Kun Li,et al.ESM-1 promotes adhesion between monocytes and endothelial cells under intermittent hypoxia[J].JOURNAL OF CELLULAR PHYSIOLOGY.2019,234(2):1512-1521.doi:10.1002/jcp.27016.
APA:
Haili Sun,Huina Zhang,Kun Li,Hao Wu,Xiaojun Zhan...&Yongxiang Wei.(2019).ESM-1 promotes adhesion between monocytes and endothelial cells under intermittent hypoxia.JOURNAL OF CELLULAR PHYSIOLOGY,234,(2)
MLA:
Haili Sun,et al."ESM-1 promotes adhesion between monocytes and endothelial cells under intermittent hypoxia".JOURNAL OF CELLULAR PHYSIOLOGY 234..2(2019):1512-1521