MiR‑29a ameliorates ischemic injury of astrocytes in vitro by targeting the water channel protein aquaporin 4.

Abstract

Ischemic stroke is the main cause of brain injury and results in a high rate of morbidity, disability and mortality. In the present study, we aimed to determine whether miR-29a played a protective role in oxygen glucose deprivation (OGD) injury via regulation of the water channel protein aquaporin 4 (AQP4). Real-time PCR and western blotting were used to assess miR-29a levels and AQP4 protein levels, respectively. Apoptosis was detected by flow cytometry, and lactate dehydrogenase (LDH) was determined by enzyme-linked immunosorbent assay (ELISA). Overexpression of miR-29a was significantly downregulated in OGD-induced primary astrocytes, and transfection with a miR-29a mimic decreased LDH release and apoptosis, and improved cell health in OGD-induced astrocytes. AQP4 was the target of miR-29a, which suppressed AQP4 expression, and knockdown of AQP4 mitigated OGD-induced astrocyte injury. Furthermore, miR-29a regulated AQP4 expression in OGD-induced astrocytes. AQP4 exacerbated astrocyte injury following ischemic stroke, and knockdown of AQP4 protected OGD/RX-induced primary cultured astrocytes against injury. The effect of miR-29a inhibitor on primary astrocytes was lost following AQP4 knockdown. These findings indicated that miR-29a prevented astrocyte injury in vitro by inhibiting AQP4. Thus, miR-29a may protect primary cultured astrocytes after OGD-induced injury by targeting AQP4, and may be a potential therapeutic target for ischemic injury of astrocytes.