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Changes in Inward Rectifier K(+) Channels in Hepatic Stellate Cells During Primary Culture

PURPOSE: This study examined the expression and function of inward rectifier K(+) channels in cultured rat hepatic stellate cells (HSC). MATERIALS AND METHODS: The expression of inward rectifier K(+) channels was measured using real-time RT-PCR, and electrophysiological properties were determined us...

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Detalles Bibliográficos
Autores principales: Lee, Dong Hyeon, Kong, In Deok, Lee, Joong-Woo, Park, Kyu-Sang
Formato: Texto
Lenguaje:English
Publicado: Yonsei University College of Medicine 2008
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2615340/
https://www.ncbi.nlm.nih.gov/pubmed/18581597
http://dx.doi.org/10.3349/ymj.2008.49.3.459
Descripción
Sumario:PURPOSE: This study examined the expression and function of inward rectifier K(+) channels in cultured rat hepatic stellate cells (HSC). MATERIALS AND METHODS: The expression of inward rectifier K(+) channels was measured using real-time RT-PCR, and electrophysiological properties were determined using the gramicidin-perforated patch-clamp technique. RESULTS: The dominant inward rectifier K(+) channel subtypes were K(ir)2.1 and K(ir)6.1. These dominant K(+) channel subtypes decreased significantly during the primary culture throughout activation process. HSC can be classified into two subgroups: one with an inward-rectifying K(+) current (type 1) and the other without (type 2). The inward current was blocked by Ba(2+) (100 µM) and enhanced by high K(+) (140 mM), more prominently in type 1 HSC. There was a correlation between the amplitude of the Ba(2+)-sensitive current and the membrane potential. In addition, Ba(2+) (300 µM) depolarized the membrane potential. After the culture period, the amplitude of the inward current decreased and the membrane potential became depolarized. CONCLUSION: HSC express inward rectifier K(+) channels, which physiologically regulate membrane potential and decrease during the activation process. These results will potentially help determine properties of the inward rectifier K(+) channels in HSC as well as their roles in the activation process.