Müller cells are closely related to diabetic retinopathy (DR). Aquaporin‐4 (AQP4) can effectively promote the diffusion of water across cellular membranes. However, the dynamic balance of water plays key role in many diseases, such as cerebral edema. Meanwhile, the unusual expression and distribution of AQP4 in the retina are the significant causes of ocular hypertension and reperfusion injury. To explore the functional significance between microRNA‐320a (miR‐320a) and AQP4 in pathological hypoxia‐induced DR related retinal edema, we hypothesized that miR‐320a regulates AQP4 expression and internalization to relieve the edema of Müller cells under the pathological retinal hypoxia stress by targeting AQP4, thereby attenuate the damage of Müller cells. Results demonstrated that miR‐320a mimics inhibited the expressions of AQP4 in Müller cells. Furthermore, overexpression miR‐320a protected Müller cells by suppressing superoxide anion. In addition, overexpression miR‐320a markedly attenuated hypoxia‐induced injury, significantly increased the cell viability, and promoted the internalization of AQP4. Furthermore, miR‐320a can also regulate the stable anchoring of AQP4 on the cell membrane. Our study indicated that miR‐320a may be a potential modulator which can mediate AQP4 expression and attenuate the hypoxia damage of Müller cells. In conclusion, miR‐320a may be a potential target for DR therapy by targeting AQP4.

中文翻译：

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microRNA-320a 通过靶向水通道蛋白 4 来防止 Müller 细胞缺氧损伤。

Müller 细胞与糖尿病视网膜病变 (DR) 密切相关。水通道蛋白-4（AQP4）可以有效促进水跨细胞膜的扩散。然而，水的动态平衡在许多疾病中起着关键作用，例如脑水肿。同时，AQP4在视网膜中的异常表达和分布是高眼压和再灌注损伤的重要原因。为了探讨microRNA-320a（miR-320a）和AQP4在病理性缺氧诱导的DR相关视网膜水肿中的功能意义，我们假设miR-320a调节AQP4的表达和内化以减轻病理性视网膜缺氧应激下Müller细胞的水肿通过靶向 AQP4，从而减轻 Müller 细胞的损伤。结果表明，miR-320a 模拟物抑制 Müller 细胞中 AQP4 的表达。此外，过度表达 miR-320a 通过抑制超氧阴离子来保护 Müller 细胞。此外，过表达miR-320a可显着减轻缺氧引起的损伤，显着增加细胞活力，并促进AQP4的内化。此外，miR-320a还可以调节AQP4在细胞膜上的稳定锚定。我们的研究表明，miR-320a可能是一种潜在的调节剂，可以介导AQP4的表达并减轻Müller细胞的缺氧损伤。总之，miR-320a 可能成为靶向 AQP4 的 DR 治疗的潜在靶点。