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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...
Autores principales: | , , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
Yonsei University College of Medicine
2008
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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 |
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author | Lee, Dong Hyeon Kong, In Deok Lee, Joong-Woo Park, Kyu-Sang |
author_facet | Lee, Dong Hyeon Kong, In Deok Lee, Joong-Woo Park, Kyu-Sang |
author_sort | Lee, Dong Hyeon |
collection | PubMed |
description | 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. |
format | Text |
id | pubmed-2615340 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2008 |
publisher | Yonsei University College of Medicine |
record_format | MEDLINE/PubMed |
spelling | pubmed-26153402009-02-02 Changes in Inward Rectifier K(+) Channels in Hepatic Stellate Cells During Primary Culture Lee, Dong Hyeon Kong, In Deok Lee, Joong-Woo Park, Kyu-Sang Yonsei Med J Original Article 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. Yonsei University College of Medicine 2008-06-30 2008-06-20 /pmc/articles/PMC2615340/ /pubmed/18581597 http://dx.doi.org/10.3349/ymj.2008.49.3.459 Text en Copyright © 2008 The Yonsei University College of Medicine http://creativecommons.org/licenses/by-nc/3.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Lee, Dong Hyeon Kong, In Deok Lee, Joong-Woo Park, Kyu-Sang Changes in Inward Rectifier K(+) Channels in Hepatic Stellate Cells During Primary Culture |
title | Changes in Inward Rectifier K(+) Channels in Hepatic Stellate Cells During Primary Culture |
title_full | Changes in Inward Rectifier K(+) Channels in Hepatic Stellate Cells During Primary Culture |
title_fullStr | Changes in Inward Rectifier K(+) Channels in Hepatic Stellate Cells During Primary Culture |
title_full_unstemmed | Changes in Inward Rectifier K(+) Channels in Hepatic Stellate Cells During Primary Culture |
title_short | Changes in Inward Rectifier K(+) Channels in Hepatic Stellate Cells During Primary Culture |
title_sort | changes in inward rectifier k(+) channels in hepatic stellate cells during primary culture |
topic | Original Article |
url | 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 |
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