Retinal Müller cells are highly polarized macroglial cells with accumulation of the aquaporin-4 (AQP4) water channel and the inwardly rectifying potassium channel Kir4.1 at specialized endfoot membrane domains abutting microvessels and corpus vitreum. Proper water and potassium homeostasis in retina depends on these membrane specializations. Here we show that targeted deletion of β1-syntrophin leads to a partial loss of AQP4 from perivascular Müller cell endfeet and that a concomitant deletion of both α1- and β1-syntrophin causes a near complete loss of AQP4 from both perivascular and subvitreal endfoot membranes. α1-syntrophin is normally very weakly expressed in Müller cell endfeet but β1-syntrophin knockout mice display an increased amount of α1-syntrophin at these sites. We suggest that upregulation of perivascular α1-syntrophin restricts the effect of β1-syntrophin deletion. The present findings indicate that β1-syntrophin plays an important role in maintaining the functional polarity of Müller cells and that α1-syntrophin can partially substitute for β1-syntrophin in AQP4 anchoring. Functional polarization of Müller cells thus depends on an interplay between two syntrophin isoforms.

中文翻译：

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视网膜Müller细胞末端的功能分工取决于两种突触素同工型之间的相互作用。

视网膜Müller细胞是高度极化的大胶质细胞，在与微血管和玻璃体邻接的特殊尾足膜区域中积累了Aquaporin-4（AQP4）水通道和向内整流钾通道Kir4.1。视网膜中适当的水和钾稳态取决于这些膜的专长。在这里，我们表明靶向缺失β1-syntrophin会导致血管周围Müller细胞末端部分丢失AQP4，同时伴随缺失α1-和β1-syntrophin会导致来自血管周围和玻璃体下足膜的AQP4几乎完全丧失。通常在Müller细胞末端中，α1-syntrophin的表达非常弱，但是敲除β1-syntrophin的小鼠在这些部位显示的α1-syntrophin数量增加。我们建议血管周围α1-syntrophin的上调限制了β1-syntrophin缺失的影响。目前的发现表明，β1-syntrophin在维持Müller细胞的功能极性方面起着重要作用，并且α1-syntrophin在AQP4锚定中可以部分替代β1-syntrophin。因此，Müller细胞的功能极化取决于两种突触素同工型之间的相互作用。