Evidence map›Paper›PMID 21874320›Full record

ArticleEndocrine2011

Ghrelin reduces voltage-gated calcium currents in GH₃ cells via cyclic GMP pathways.

Xuefeng Han, Yunlong Zhu, Yufeng Zhao, Chen Chen

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In one paragraph

Article in Endocrine, 2011. 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
–field-weighted citation impact
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.

  1. Article
  2. Potassium Current Is Not Affected by Long-Term Exposure to Ghrelin or GHRP-6 in Somatotropes GC Cells.Journal of biophysics (Hindawi Publishing Corporation : Online) · 2013
    Article
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.

Xuefeng HanDepartment of Physiology, Fourth Military Medical University, Shannxi, China.
Yunlong Zhu
Yufeng Zhao
Chen Chen

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ghrelin is an endogenous growth hormone secretagogue (GHS) causing release of GH from pituitary somatotropes through the GHS receptor. Secretion of GH is linked directly to intracellular free Ca2+ concentration ([Ca2+]i), which is determined by Ca2+ influx and release from intracellular Ca2+ storage sites. Ca2+ influx is via voltage-gated Ca2+ channels, which are activated by cell depolarization. The mechanism underlying the effect of ghrelin on voltage-gated Ca2+ channels is still not clear. In this report, using whole cell patch-clamp recordings, we assessed the acute action of ghrelin on voltage-activated Ca2+ currents in GH3 rat somatotrope cell line. Ca2+ currents were divided into three types (T, N, and L) through two different holding potentials (-80 and -40 mV) and specific L-type channel blocker (nifedipine, NFD). We demonstrated that ghrelin significantly and reversibly decreases all three types of Ca2+ currents in GH3 cells through GHS receptors on the cell membrane and down-stream signaling systems. With different signal pathway inhibitors, we observed that ghrelin-induced reduction in voltage-gated Ca2+ currents in GH3 cells was mediated by a protein kinase G-dependent pathways. As ghrelin also stimulates Ca2+ release and prolongs the membrane depolarization, this reduction in voltage-gated Ca2+ currents may not be translated into a reduction in [Ca2+]i, or a decrease in GH secretion.

Indexed as

Second Messenger SystemsAnimalsCalcium Channel BlockersCalcium ChannelsCalcium Channels, L-TypeCalcium Channels, N-TypeCalcium Channels, T-TypeCalcium SignalingCell LineCyclic GMPCyclic GMP-Dependent Protein KinasesGhrelinMembrane PotentialsNifedipinePatch-Clamp TechniquesProtein Kinase CCalcium Channel BlockersCalcium ChannelsCalcium Channels, L-TypeCalcium Channels, N-TypeCalcium Channels, T-TypeCyclic GMPCyclic GMP-Dependent Protein KinasesGhrelinNifedipineProtein Kinase CProtein Kinase InhibitorsReceptors, Ghrelin

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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.