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Expression and high glucose-mediated regulation of K+ channel interacting protein 3 (KChIP3) and KV4 channels in retinal Muller glial cells.

Authors: Chavira-Suarez, E  Sandoval, A  Felix, R  Lamas, M 
Citation: Chavira-Suarez E, etal., Biochem Biophys Res Commun. 2011 Jan 14;404(2):678-83. doi: 10.1016/j.bbrc.2010.12.041. Epub 2010 Dec 11.
Pubmed: (View Article at PubMed) PMID:21147063
DOI: Full-text: DOI:10.1016/j.bbrc.2010.12.041

Normal vision depends on the correct function of retinal neurons and glia and it is impaired in the course of diabetic retinopathy. Muller cells, the main glial cells of the retina, suffer morphological and functional alterations during diabetes participating in the pathological retinal dysfunction. Recently, we showed that Muller cells express the pleiotropic protein potassium channel interacting protein 3 (KChIP3), an integral component of the voltage-gated K(+) channels K(V)4. Here, we sought to analyze the role of KChIP3 in the molecular mechanisms underlying hyperglycemia-induced phenotypic changes in the glial elements of the retina. The expression and function of KChIp3 was analyzed in vitro in rat Muller primary cultures grown under control (5.6 mM) or high glucose (25 mM) (diabetic-like) conditions. We show the up-regulation of KChIP3 expression in Muller cell cultures under high glucose conditions and demonstrate a previously unknown interaction between the K(V)4 channel and KChIP3 in Muller cells. We show evidence for the expression of a 4-AP-sensitive transient outward voltage-gated K(+) current and an alteration in the inactivation of the macroscopic outward K(+) currents expressed in high glucose-cultured Muller cells. Our data support the notion that induction of KChIP3 and functional changes of K(V)4 channels in Muller cells could exert a physiological role in the onset of diabetic retinopathy.


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CRRD Object Information
CRRD ID: 7207197
Created: 2013-01-23
Species: All species
Last Modified: 2013-01-23
Status: ACTIVE


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