Abstract
We have demonstrated that neural progenitor cells (NPCs) protect endothelial cells (ECs) from oxidative stress. Since exosomes (EXs) can convey the benefit of parent cells through their carried microRNAs (miRs) and miR-210 is ubiquitously expressed with versatile functions, we investigated the role of miR-210 in the effects of NPC-EXs on oxidative stress and dysfunction in ECs. NPCs were transfected with control and miR-210 scramble/inhibitor/mimic to generate NPC-EXscon, NPC-EXssc, NPC-EXsanti-miR-210, and NPC-EXsmiR-210. The effects of various NPC-EXs on angiotensin II- (Ang II-) induced reactive oxygen species (ROS) overproduction, apoptosis, and dysfunction, as well as dysregulation of Nox2, ephrin A3, VEGF, and p-VEGFR2/VEGFR2 in ECs were evaluated. Results showed (1) Ang II-induced ROS overproduction, increase in apoptosis, and decrease in tube formation ability, accompanied with Nox2 upregulation and reduction of p-VEGFR2/VEGFR2 in ECs. (2) Compared to NPC-EXscon or NPC-EXssc, NPC-EXsanti-miR-210 were less whereas NPC-EXsmiR-210 were more effective on attenuating these detrimental effects induced by Ang II in ECs. (3) These effects of NPC-EXsanti-miR-210 and NPC-EXsmiR-210 were associated with the changes of miR-210, ephrin A3, VEGF, and p-VEGFR2/VEGFR2 ratio in ECs. Altogether, the protective effects of NPC-EXs on Ang II-induced endothelial injury through miR-210 which controls Nox2/ROS and VEGF/VEGFR2 signals were studied.
Highlights
Oxidative stress is well-known to play a critical role in a diverse array of cardiovascular disorders including hypertension, diabetic vasculopathy, hypercholesterolemia, and atherosclerosis [1,2,3]
In order to explore the mechanism of neural progenitor cells (NPCs) protecting endothelial cells (ECs) from oxidative stress, we investigated whether EXs released from NPCs (NPC-EXs) can protect ECs from oxidative stress and dysfunction in an angiotensin II- (Ang II-)induced injury model
We have demonstrated that NPC-EXs have protective effects against Ang II-induced oxidative stress, cell death, and angiogenic dysfunction in ECs, which p-VEGFR2/VEGFR2
Summary
Oxidative stress is well-known to play a critical role in a diverse array of cardiovascular disorders including hypertension, diabetic vasculopathy, hypercholesterolemia, and atherosclerosis [1,2,3]. Endothelial progenitor cell-derived vesicles can protect ECs against hypoxia/reoxygenation injury [16]. Our group demonstrated that endothelial progenitor cell-derived vesicles from healthy controls have protective effects on the function of endothelial progenitor cells from diabetic patients through their carried miR-126 [14]. Wang et al reported that EXs derived from inducible pluripotent stem cells can deliver miR-210 to the cardiomyocytes and protect the cardiomyocytes against H2O2-induced oxidative stress [15]. There is no study investigating whether miR-210 is involved in the protective effects of NPC-EXs on ECs against oxidative stress. We illustrated whether miR-210 participates in the protective effects of NPC-EXs on attenuating Ang IIinduced ROS overproduction and dysfunction in ECs
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
