Exosome-transported Long Non-coding Ribonucleic Acid H19 Induces Blood-brain Barrier Disruption in Cerebral Ischemic Stroke Via the H19/micro Ribonucleic Acid-18a/Vascular Endothelial Growth factor Axis

被引:16
作者
Wang, Jue [1 ]
Cao, Bin [1 ]
Sun, Ruize [1 ]
Chen, Yuhua [2 ,3 ]
Feng, Juan [1 ]
机构
[1] China Med Univ, Dept Neurol, Shengjing Hosp, Sanhao St, Shenyang 110004, Peoples R China
[2] China Med Univ, Dept Dev Cell Biol, Key Lab Cell Biol, Minist Publ Hlth, Shenyang, Peoples R China
[3] China Med Univ, Key Lab Med Cell Biol, Minist Educ, Shenyang, Peoples R China
基金
中国国家自然科学基金;
关键词
Long non-coding RNA; H19; Cerebral ischemic stroke; Exosomes; Blood-brain barrier; RNA; PROGRESSION; ASTROCYTES; ACTIVATION; INJURY;
D O I
10.1016/j.neuroscience.2022.07.028
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Long non-coding RNA H19 (lncRNA H19) is transcribed from the H19 gene. We previously reported the role of lncRNA H19 in the pathogenesis of cerebral ischemic stroke. The present study aimed to elucidate the relationship between lncRNA H19 and blood-brain barrier breakdown induced by cerebral ischemic stroke. We observed that plasma levels of lncRNA H19 were positively associated with the extent of blood-brain barrier damage. In cellular co-culture models, neurons expressed and transported lncRNA H19 to astrocytes via exosomes and contributed to an increase in endothelium permeability induced by oxygen-glucose deprivation. Inhibition of neuronal exosomal lncRNA H19 regulated astrocytic microRNA (miR)-18a and vascular endothelial growth factor (VEGF) expression. Further, lncRNA H19 induced a decrease in tight junction proteins expression via the lncRNA H19/miR-18a/VEGF axis. This study highlights the transportation of lncRNA H19 by exosomes and the relationship between lncRNA H19 and blood-brain barrier breakdown. (C) 2022 Published by Elsevier Ltd on behalf of IBRO.
引用
收藏
页码:41 / 51
页数:11
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