Exosomal lncRNA ENST00000592016 rescues the Weakened Viability of HUVEC Cells Caused by Intermittent Hypoxia

Obstructive sleep apnea syndrome [OSAS] is a common sleep breathing disorder accompanied by multiple organ intermittent hypoxemia. Our previous study has suggested that the expression of a lncRNA termed ENST00000592016 [lnc2016 for short] derived from plasma exosomes is remarkably elevated in OSA patients compared to the normal population, and lnc2016 can improve the diagnostic efficiency of OSA.

To unmask the role of the lnc2016 in vascular endothelial cells, targeted hypoxia is the goal of the current research.

Primary human ADSCs and HUVEC cells were cultured. CCK-8, cytometric assay, transwell, and tubular formation assay were used to determine cell viability, cell apoptosis, cell cycle, cell migration, as well as tubular formation ability.

Adipose-derived stem cells [ADSCs]-derived exosomes contained robust lnc2016. After co-culture with human umbilical vein endothelial cells [HUVECs], exosomal lnc2016 could enhance cell proliferation, DNA synthesis, migration, and tubular formation, whereas suppress cell apoptosis of HUVECs against hypoxic conditions.

Under hypoxic conditions, ADSCs secrete various reparative factors and transmit them via exosomes; among them, lnc2016 may participate in the regulation of hypoxia-induced injury through the ceRNA network, which requires further investigation.

Ln2016 can promote the cell growth, migration, DNA synthesis, and tubular formation as well as suppress the cell apoptosis of vascular endothelial cells against hypoxia in vitro.