Circular RNAs (circRNAs) play regulatory roles in cerebrovascular disease. Human brain microvascular endothelial cells (HBMECs) are involved in cerebrovascular dysfunction in ischemic stroke. Here, researchers investigated the role of circ_0000566 in oxygen-glucose deprivation/reoxygenation (OGD/R)-induced HBMECs. Results showed that circ_0000566 and ACVR2B were highly expressed, whereas miR-18a-5p was downregulated in OGD/R-treated HBMECs. OGD/R treatment promoted apoptosis and inflammation in HBMECs and inhibited cell viability, whereas silencing circ_0000566 mitigated these effects. Circ_0000566, acting as a sponge for miR-18a-5p, was involved in OGD/R-induced HBMEC damage. ACVR2B is a direct target of miR-18a-5p. ACVR2B overexpression may abrogate the inhibitory effect of miR-18a-5p on OGD/R-treated HBMECs injury. Circ_0000566 sponged miR-18a-5p to regulate OGD/R-induced HBMECs injury via regulating ACVR2B expression.
Here, researchers investigated the role of ACVR2B in OGD/R-induced HBMEC injury. Transfection of HBMECs with si-ACVR2B significantly reduced ACVR2B protein expression (Figure 1A). Furthermore, OGD/R-induced ACVR2B expression was inhibited by si-ACVR2B transfection (Figure 1B). ACVR2B knockdown in OGD/R-induced HBMECs increased cell viability and Bcl-2 protein levels, while inhibiting LDH release, apoptosis rate, and protein expression of Bax, c-caspase 3, and c-caspase 9 (Figures 1C-J). Furthermore, ACVR2B knockdown also reduced IL-1β, IL-6, and TNF-α levels in OGD/R-induced HBMECs (Figures 1K-M). These data confirm that ACVR2B knockdown alleviates OGD/R-induced HBMEC injury.
Figure 1. ACVR2B regulated OGD/R-stimulated HBMEC damage. (Liu D, et al., 2023)