Changes in Inward Rectifier K+ Channels in Hepatic Stellate Cells During Primary Culture
This study examined the expression and function of inward rectifier K(+) channels in cultured rat hepatic stellate cells (HSC). The expression of inward rectifier K(+) channels was measured using real-time RT-PCR, and electrophysiological properties were determined using the gramicidin-perforated pa...
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Published in | Yonsei medical journal Vol. 49; no. 3; pp. 459 - 471 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Korea (South)
Yonsei University College of Medicine
30.06.2008
연세대학교의과대학 |
Subjects | |
Online Access | Get full text |
ISSN | 0513-5796 1976-2437 |
DOI | 10.3349/ymj.2008.49.3.459 |
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Summary: | This study examined the expression and function of inward rectifier K(+) channels in cultured rat hepatic stellate cells (HSC).
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.
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 microM) 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 microM) depolarized the membrane potential. After the culture period, the amplitude of the inward current decreased and the membrane potential became depolarized.
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. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 G704-000409.2008.49.3.022 http://kmbase.medric.or.kr/Main.aspx?d=KMBASE&m=VIEW&i=0311120080490030459 |
ISSN: | 0513-5796 1976-2437 |
DOI: | 10.3349/ymj.2008.49.3.459 |