Aquaporin-1 expression and conventional aqueous outflow in human eyes.

Aquaporin-1 expression and conventional aqueous outflow in human eyes.
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DOI:
10.1016/j.exer.2008.06.018
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发表时间:
2008-10
影响因子:
3.4
通讯作者:
Ethier, C. Ross
Ethier, C. Ross
中科院分区:
医学3区
文献类型:
--
作者:
Stamer, W. Daniel;Chan, Darren W. H.;Conley, Shannon M.;Coons, Serena;Ethier, C. Ross

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水通道蛋白通道促进分泌和吸收组织对水的渗透性增强。在常规排水道中,水通道蛋白-1表达,但其对流出设施的贡献尚不清楚。本研究的目的是确定人体常规排水通路细胞水通道蛋白-1表达升高对流出设施的影响。利用器官培养的13对人前段,利用腺病毒编码人水通道蛋白-1修饰流出细胞中水通道蛋白-1的表达。对侧前节段作为对照,用腺病毒编码β -半乳糖苷酶进行转导。通过共聚焦免疫荧光显微镜,我们观察到,与内源性水平相比,暴露于腺病毒(在灌注期间通过注射到进管中)的前段小梁内网细胞的水通道蛋白-1表达增加。相比之下,外网细胞(关节旁区)和施莱姆管中水通道蛋白-1的升高需要通过锁膜外静脉的后灌注将腺病毒转导到前节段。无论暴露途径如何,实验段的流出设施与对照组没有差异。具体来说,内部网络中水通道蛋白-1的过表达导致了- 2.0±9.2%的平均设施变化,而在阻力产生区域中水通道蛋白-1的过表达使流出设施改变了- 3.2±11.2%。综上所述,这些结果表明,由水通道蛋白-1介导的跨细胞途径对人眼常规水流出道的大量流出没有显著贡献。
Aquaporin channels facilitate the enhanced permeability of secretory and absorptive tissues to water. In the conventional drainage tract, aquaporin-1 is expressed but its contribution to outflow facility is unknown. The purpose of the present study was to determine the effect of elevated aquaporin-1 expression by cells of the human conventional drainage pathway on outflow facility. Using thirteen pairs of human anterior segments in organ culture, we modified aquaporin-1 protein expression in outflow cells using adenovirus encoding human aquaporin-1. Contralateral anterior segments served as controls and were transduced with adenovirus encoding beta galactosidase. By confocal immunofluorescence microscopy, we observed that inner trabecular meshwork cells from anterior segments exposed to adenovirus (via injection into the inlet tubing during perfusion) had increased aquaporin-1 protein expression compared to endogenous levels. In contrast, elevation of aquaporin-1 protein in outer meshwork cells (juxtacanalicular region) and Schlemm’s canal required transduction of adenovirus into anterior segments using retroperfusion via episcleral veins. Regardless of exposure route, outflow facility of experimental segments was not different than control. Specifically, overexpression of aquaporin-1 in the inner meshwork resulted in an average facility change of −2.0 ± 9.2 %, while overexpression of aquaporin-1 in the resistance-generating region changed outflow facility by −3.2 ± 11.2 %. Taken together, these results indicate that a transcellular pathway, mediated by aquaporin-1, does not contribute significantly to bulk outflow through the conventional aqueous outflow tract of human eyes.
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