Evidence map›Paper›PMID 18581597›Full record

ArticleYonsei medical journal2008

Changes in inward rectifier K+ channels in hepatic stellate cells during primary culture.

Dong Hyeon Lee, In Deok Kong, Joong-Woo Lee, Kyu-Sang Park

Open access · goldAbstract read
In one paragraph

Article in Yonsei medical journal, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 41% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Dong Hyeon LeeDepartment of Physiology, College of Medicine, Pochon CHA University, Seongnam, Gyeonggi-do, Korea.
In Deok Kong
Joong-Woo Lee
Kyu-Sang Park
Yonsei University · KRCHA University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeThis study examined the expression and function of inward rectifier K(+) channels in cultured rat hepatic stellate cells (HSC). MATERIALS AND

methodsThe 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.

resultsThe 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.

conclusionHSC 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.

Indexed as

AnimalsBariumBlotting, WesternCells, CulturedElectrophysiologyLiverMaleMembrane PotentialsPotassiumPotassium Channels, Inwardly RectifyingRatsRats, Sprague-DawleyReverse Transcriptase Polymerase Chain ReactionBariumPotassiumPotassium Channels, Inwardly Rectifying

Identifiers

PMID18581597
PMCPMC2615340
OpenAlexW2144549662

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.