Delayed peripheral nerve rehabilitation in aquaporin-3 deficiency in mouse models of sciatic nerve contusion.

Neuro endocrinology letters Pub Date : 2025-04-28
Jie Wang, Sixuan Li, Hong Huang, Yixuan Wang, Miao Li
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Abstract

Background: Aquaporin-3 (AQP3) water channels are belonging to the aquaporin water channel family, permeable not only to water but also to some small solutes such as glycerol and lactate. The purpose of this study is to investigate the possible functions of AQP3 in peripheral nerve rehabilitation based on AQP3-deficient mice.

Methods: Mature 8-week-old female AQP3-deficient (AQP3-/-) mice and C57BL/6 (WT) mice initially weighing 25~30 g were used in this study. Schwann cells were isolated from sciatic nerves of WT and AQP3-/- mice respectively. AQP3 mRNA and protein expression in sciatic nerve tissues and Schwann cells were detected by RT-PCR, immunoblot analysis, and immunofluorescence staining. Sciatic nerve cross sections from the WT and AQP3-/- mice were stained by toluidine-blue agent to identify the potential influence of AQP3 deficiency to the morphology nerve fibers. The proliferation and migration ability of AQP3-/- and WT Schwann cells were observed in primary cell cultures. To explore the possible role of AQP3 in nerve repair processes, sciatic nerve contusion models were established and walking track analysis was performed on both WT and AQP3-/- mice.

Results: AQP3 was localized in the membrane of Schwann cells. AQP3-deficiency did not alter the morphology of fibers in the sciatic nerve. There was an increase of AQP3 protein expression in the sciatic nerve of wild-type mice after injury. Primary culture of Schwann cells and in vitro wound healing model revealed that AQP3-deficient Schwann cells exhibited the same morphology, while showing lower proliferation and migration ability compared with wild-type Schwann cells. There was obvious delay in motor function rehabilitation in AQP3-deficient mice compared with that of wild-type mice.

Conclusion: Our study suggested that AQP3 localized in the membrane of Schwann cells and facilitated Schwann cells' proliferation and migration. AQP3 deficiency impaired nerve rehabilitation in wound healing model both in vitro and in vivo. The study support our hypothesis that AQP3 participates in myelin damnification and repair course and the mechanisms underlying the AQP3 in the field of myelin repair and regeneration in peripheral nerves deserves further investigation and exploration in detail.

坐骨神经损伤小鼠模型水通道蛋白-3缺乏症导致周围神经延迟康复。
背景:水通道蛋白-3 (aquaporin -3, AQP3)是水通道蛋白家族的一员,不仅对水具有渗透性,而且对甘油、乳酸等小溶质也具有渗透性。本研究的目的是基于AQP3缺陷小鼠,探讨AQP3在周围神经康复中的可能功能。方法:以8周龄成熟雌性AQP3-/-缺失(AQP3-/-)小鼠和体重25~30 g的C57BL/6 (WT)小鼠为研究对象。分别从WT和AQP3-/-小鼠坐骨神经中分离雪旺细胞。采用RT-PCR、免疫印迹和免疫荧光染色检测坐骨神经组织和雪旺细胞中AQP3 mRNA和蛋白的表达。用甲苯胺蓝染色WT和AQP3-/-小鼠坐骨神经横断面,以确定AQP3缺乏对神经纤维形态的潜在影响。在原代细胞培养中观察AQP3-/-和WT雪旺细胞的增殖和迁移能力。为了探讨AQP3在神经修复过程中的可能作用,我们建立了坐骨神经挫伤模型,并对WT和AQP3-/-小鼠进行了步行轨迹分析。结果:AQP3定位于雪旺细胞膜。aqp3缺乏未改变坐骨神经纤维形态。野生型小鼠坐骨神经损伤后AQP3蛋白表达增加。雪旺细胞原代培养和体外创面愈合模型显示,aqp3缺失的雪旺细胞形态相同,但与野生型雪旺细胞相比,增殖和迁移能力较低。与野生型小鼠相比,aqp3缺陷小鼠运动功能恢复明显延迟。结论:我们的研究表明AQP3定位于雪旺细胞的细胞膜,促进了雪旺细胞的增殖和迁移。体外和体内研究表明,AQP3缺乏对创伤愈合模型的神经康复均有影响。本研究支持了我们关于AQP3参与髓鞘损伤修复过程的假设,AQP3在周围神经髓鞘修复和再生中的作用机制值得进一步深入研究和探索。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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