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

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.

Automated summary

This study elucidates the relationship between the transport of lncRNA H19 by exosomes and blood-brain barrier breakdown induced by cerebral ischemic stroke.