Evidence map›Paper›PMID 18272248›Full record

ArticleJournal of hepatology2008

Augmenter of liver regeneration: an important intracellular survival factor for hepatocytes.

Chinnasamy Thirunavukkarasu, Lian Fu Wang, Stephen A K Harvey, Simon C Watkins, J Richard Chaillet, John Prelich, Thomas E Starzl, Chandrashekhar R Gandhi

Open access · hybridAbstract readComparative Study
In one paragraph

Article in Journal of hepatology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

36 citing papers in PubMed, 78 citations in OpenAlex.

  1. Article
  2. Article
  3. Observational
  4. Review
  5. Article
  6. 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
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. 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
  17. Article
  18. Article
  19. Article
  20. 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

8 authors at 2 institutions in 1 country.

Chinnasamy ThirunavukkarasuDepartment of Surgery, Thomas E. Starzl Transplantation Institute, University of Pittsburgh, E-1542 BST, 200 Lothrop Street, Pittsburgh, PA 15213, USA.
Lian Fu Wang
Stephen A K Harvey
Simon C Watkins
J Richard Chaillet
John Prelich
Thomas E Starzl
Chandrashekhar R Gandhi
University of Pittsburgh · USUniversity of Pittsburgh Medical Center · US

Funding

ORTHOTOPIC LIVER TRANSPLANTATIONR01DK029961 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI STARZL, THOMAS E · 1986 to 2001
$876k
NIDDK NIH HHS R01 DK029961
6 · The paper itself

Abstract

BACKGROUND/

aimsAugmenter of liver regeneration (ALR), a protein synthesized and stored in hepatocytes, is associated with mitochondria, and possesses sulfhydryl oxidase and cytochrome c reductase activities. We sought to determine the effects of ALR depletion in hepatocytes by antisense oligonucleotide transfection.

methodsRat hepatocytes in primary culture were transfected with antisense oligonucleotide for ALR mRNA (ALR-AS) or scrambled oligonucleotide. Various analyses were performed at times up to 24h after transfection.

resultsTreatment with ALR-AS caused a decrease in ALR mRNA, cellular depletion of ALR protein primarily from mitochondria, and decreased viability. Flow cytometric analysis of ALR-AS-transfected hepatocytes stained with annexin-Vcy3 and 7-aminoactinomycin D revealed apoptosis as the predominant cause of death up to 6h; incubation beyond this time resulted in necrosis in addition to apoptosis. ALR-AS-transfection caused release of mitochondrial cytochrome c, activation of caspase-3, profound reduction in the ATP content, and cellular release of LDH. Inhibition of caspase-3 inhibited the early phase of ALR-AS-induced death but not the late phase that included ALR and LDH release.

conclusionsThese results suggest that ALR is critically important for the survival of hepatocytes by its association with mitochondria and regulation of ATP synthesis.

Indexed as

Adenosine TriphosphateAnimalsApoptosisCell CountCells, CulturedCell SurvivalFlow CytometryHepatocytesIntracellular FluidMitochondria, LiverOligonucleotides, AntisenseOxidoreductases Acting on Sulfur Group DonorsProteinsRatsReverse Transcriptase Polymerase Chain ReactionRNA, MessengerAdenosine TriphosphateGFER protein, ratOligonucleotides, AntisenseOxidoreductases Acting on Sulfur Group DonorsProteinsRNA, Messenger

Identifiers

PMID18272248
PMCPMC2954779
OpenAlexW2034533835

What OpenQuestion holds

Textmetadata
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.