Kir7.1 inwardly rectifying K + channel is expressed in ciliary body non pigment epithelial cells and might contribute to intraocular pressure regulation.

Autor: Burgos J; Centro de Estudios Científicos (CECs), Avenida Arturo Prat 514, Valdivia, Chile., Villanueva S; Centro de Estudios Científicos (CECs), Avenida Arturo Prat 514, Valdivia, Chile; Universidad Austral de Chile, Valdivia, Chile., Ojeda M; Centro de Estudios Científicos (CECs), Avenida Arturo Prat 514, Valdivia, Chile., Cornejo I; Centro de Estudios Científicos (CECs), Avenida Arturo Prat 514, Valdivia, Chile., Cid LP; Centro de Estudios Científicos (CECs), Avenida Arturo Prat 514, Valdivia, Chile., Sepúlveda FV; Centro de Estudios Científicos (CECs), Avenida Arturo Prat 514, Valdivia, Chile. Electronic address: fsepulveda@cecs.cl.
Jazyk: angličtina
Zdroj: Experimental eye research [Exp Eye Res] 2019 Sep; Vol. 186, pp. 107723. Date of Electronic Publication: 2019 Jul 15.
DOI: 10.1016/j.exer.2019.107723
Abstrakt: Inwardly rectifying K + channel Kir7.1 is expressed in epithelia where it shares membrane localisation with the Na + /K + -pump. The ciliary body epithelium (CBE) of the eye is a determinant of intraocular pressure (IOP) through NaCl-driven fluid secretion of aqueous humour. In the present study we explored the presence Kir7.1 in this epithelium in the mouse and its possible functional role in the generation of IOP. Use heterozygous animals for total Kir7.1 knockout expressing β-galactosidase under the control of Kir7.1 promoter, identified the expression of Kir7.1 in non-pigmented epithelial cells of CBE. Using conditional, floxed knockout Kir7.1 mice as negative controls, we found Kir7.1 at the basolateral membrane of the same CBE cell layer. This was confirmed using a knockin mouse expressing the Kir7.1 protein tagged with a haemagglutinin epitope. Measurements using the conditional knockout mouse show only a minor effect of Kir7.1 inactivation on steady-state IOP. Transient increases in IOP in response to general anaesthetics, or to water injection, are absent or markedly curtailed in Kir7.1-deficient mice. These results suggest a role for Kir7.1 in IOP regulation through a possible modulation of aqueous humour production by the CBE non-pigmented epithelial cells. The location of Kir7.1 in the CBE, together with the effect of its removal on dynamic changes in IOP, point to a possible role of the channel as a leak pathway preventing cellular overload of K + during the secretion process. Kir7.1 could be used as a potential therapeutic target in pathological conditions leading to elevated intraocular pressure.
(Copyright © 2019 Elsevier Ltd. All rights reserved.)
Databáze: MEDLINE
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