Iandiev Ianors, Pannicke Thomas, Biedermann Bernd, Wiedemann Peter, Reichenbach Andreas, Bringmann Andreas
Paul Flechsig Institute of Brain Research, University of Leipzig Medical Faculty, 04109 Leipzig, Germany.
Neurosci Lett. 2006 Nov 13;408(2):108-12. doi: 10.1016/j.neulet.2006.08.084. Epub 2006 Sep 25.
Glial cells control the retinal osmohomeostasis, in part via mediation of water fluxes through aquaporin (AQP) water channels. By using immunohistochemical staining, we investigated whether ischemia-reperfusion of the rat retina causes alterations in the distribution of AQP1 and AQP4 proteins. Transient ischemia was induced in retinas of Long-Evans rats by elevation of the intraocular pressure for 60 min. In control retinas, immunoreactive AQP1 was expressed in the outer retina and by distinct amacrine cells, and AQP4 was expressed by glial cells (Müller cells and astrocytes) predominantly in the inner retina. After ischemia, retinal glial cells in the nerve fiber/ganglion cell layers strongly expressed AQP1. The perivascular staining around the superficial vessels altered from AQP4 in control retinas to AQP1 in postischemic retinas. The data suggest that the glial cell-mediated water transport in the retina is altered after ischemia especially at the superficial vessel plexus.
神经胶质细胞部分通过水通道蛋白(AQP)水通道介导水通量来控制视网膜的渗透稳态。通过免疫组织化学染色,我们研究了大鼠视网膜缺血再灌注是否会导致AQP1和AQP4蛋白分布的改变。通过升高眼内压60分钟,在Long-Evans大鼠的视网膜中诱导短暂性缺血。在对照视网膜中,免疫反应性AQP1在外层视网膜和不同的无长突细胞中表达,而AQP4主要在内层视网膜的神经胶质细胞(穆勒细胞和星形胶质细胞)中表达。缺血后,神经纤维/神经节细胞层中的视网膜神经胶质细胞强烈表达AQP1。浅层血管周围的血管周围染色从对照视网膜中的AQP4变为缺血后视网膜中的AQP1。数据表明,缺血后视网膜中神经胶质细胞介导的水转运发生改变,尤其是在浅层血管丛处。