Evidence map›Paper›PMID 19859909›Full record

ArticleJournal of cellular physiology2010

Cholera toxin-sensitive GTP-binding protein-coupled activation of augmenter of liver regeneration (ALR) receptor and its function in rat kupffer cells.

Chandrashekhar R Gandhi, Noriko Murase, Thomas E Starzl

Open access · greenAbstract read
In one paragraph

Article in Journal of cellular physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

16 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Augmenter of liver regeneration protein deficiency promotes hepatic steatosis by inducing oxidative stress and microRNA-540 expression.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  5. Review
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  7. Article
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  9. Knockdown of augmenter of liver regeneration in HK-2 cells inhibits inflammation response via the mitogen-activated protein kinase signaling pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2015
    Article
  10. Article
  11. Article
  12. Article
  13. Augmenter of liver regeneration.Fibrogenesis & tissue repair · 2012
    Article
  14. Article
  15. Article
  16. 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

3 authors at 1 institution in 1 country.

Chandrashekhar R GandhiVA Pittsburgh Healthcare System, Pittsburgh, Pennsylvania, USA. gandhics@msx.upmc.edu
Noriko Murase
Thomas E Starzl
University of Pittsburgh · US

Funding

ROLE OF STELLATE CELLS IN LIVER FAILURER01DK054411 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GANDHI, CHANDRASHEKHAR R · 1998 to 2006
$1.7M
ORTHOTOPIC LIVER TRANSPLANTATIONR01DK029961 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI STARZL, THOMAS E · 1986 to 2001
$876k
NIDDK NIH HHS DK 54411NIDDK NIH HHS R01 DK029961NIDDK NIH HHS R01 DK054411
6 · The paper itself

Abstract

Mitogenic effect of augmenter of liver regeneration (ALR), a protein produced and released by hepatocytes, on hepatocytes in vivo but not in vitro suggests that the effect is mediated by nonparenchymal cells. Since mediators produced by Kupffer cells are implicated in hepatic regeneration, we investigated receptor for ALR and its functions in rat Kupffer cells. Kupffer cells were isolated from rat liver by enzymatic digestion and centrifugal elutriation. Radioligand ([(125)I] ALR) receptor binding, ALR-induced GTP/G-protein association, and nitric oxide (NO), tumor necrosis factor (TNF)-alpha, and interleukin-6 (IL-6) synthesis were determined. High-affinity receptor for ALR, belonging to the G-protein family, with K(d) of 1.25 +/- 0.18 nM and B(max) of 0.26 +/- 0.02 fmol/microg DNA was identified. ALR stimulated NO, TNF-alpha, and IL-6 synthesis via cholera toxin-sensitive G-protein, as well as p38-MAPK activity and nuclear translocation of NFkappaB. While inhibitor of NFkappaB (MG132) inhibited ALR-induced NO synthesis, MG132 and p38-MAPK inhibitor (SB203580) abrogated ALR-induced TNF-alpha and IL-6 synthesis. ALR also prevented the release of mediator(s) from Kupffer cells that cause inhibition of DNA synthesis in hepatocytes. Administration of ALR to 40% partially hepatectomized rats increased expression of TNF-alpha, IL-6, and inducible nitric oxide synthase (iNOS) and caused augmentation of hepatic regeneration. These results demonstrate specific G-protein coupled binding of ALR and its function in Kupffer cells and suggest that mediators produced by ALR-stimulated Kupffer cells may elicit physiologically important effects on hepatocytes.

Indexed as

Liver RegenerationAnimalsCell ProliferationCholera ToxinHepatectomyHepatocytesImidazolesInterleukin-6Kupffer CellsLeupeptinsLiverMaleNF-kappa BNitric OxideNitric Oxide Synthase Type IIOxidoreductases Acting on Sulfur Group Donorsbenzyloxycarbonylleucyl-leucyl-leucine aldehydeCholera ToxinGFER protein, ratImidazolesInterleukin-6LeupeptinsNF-kappa BNitric OxideNitric Oxide Synthase Type IINos2 protein, ratOxidoreductases Acting on Sulfur Group Donorsp38 Mitogen-Activated Protein KinasesProtein Kinase InhibitorsProteinsPyridinesReceptors, G-Protein-CoupledRNA, MessengerSB 203580Tumor Necrosis Factor-alpha

Identifiers

PMID19859909
PMCPMC3034370
OpenAlexW2144541338

What OpenQuestion holds

Textmetadata
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Read underepoch 390

Registered trials

None linked

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.