Evidence map›Paper›PMID 21514425›Full record

ArticleThe American journal of pathology2011

Thymosin-β4 (Tβ4) blunts PDGF-dependent phosphorylation and binding of AKT to actin in hepatic stellate cells.

Karina Reyes-Gordillo, Ruchi Shah, Anastas Popratiloff, Sidney Fu, Anna Hindle, Frederick Brody, Marcos Rojkind

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

22 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. The Role of Tβ4-POP-Ac-SDKP Axis in Organ Fibrosis.International journal of molecular sciences · 2022
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. ThymosinOxidative medicine and cellular longevity · 2018
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Potential role of thymosin Beta 4 in liver fibrosis.International journal of molecular sciences · 2015
    Review
  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

7 authors at 1 institution in 1 country.

Karina Reyes-GordilloDepartment of Biochemistry and Molecular Biology, The George Washington University Medical Center, Washington, DC, USA.
Ruchi Shah
Anastas Popratiloff
Sidney Fu
Anna Hindle
Frederick Brody
Marcos Rojkind
George Washington University · US

Funding

PHS HHS R01 10541
6 · The paper itself

Abstract

Hepatic stellate cell transdifferentiation is a key event in the fibrogenic cascade. Therefore, attempts to prevent and/or revert the myofibroblastic phenotype could result in novel therapeutic approaches to treat liver cirrhosis. The expression of platelet-derived growth factor (PDGF)-β receptor and the proliferative response to platelet-derived growth factor-ββ (PDGF-ββ) are hallmarks of the transdifferentiation of hepatic stellate cells (HSC). In this communication, we investigated whether thymosin-β4 (Tβ4), a chemokine expressed by HSC could prevent PDGF-BB-mediated proliferation and migration of cultured HSC. Using early passages of human HSC, we showed that Tβ4 inhibited cell proliferation and migration and prevented the expression of PDGF-β receptor (PDGF-βr), α-smooth muscle actin and α1(I) collagen mRNAs. Tβ4 also inhibited the reappearance of PDGF-βr after its PDGF-BB-dependent degradation. These PDGF-dependent events were associated with the inhibition of AKT phosphorylation at both T308 and S473 amino acid residues. The lack of AKT phosphorylation was not due to the inhibition of PDGF-βr phosphorylation, the activation of phosphoinositide 3-kinase (PI3K), pyruvate dehydrogenase kinase isozyme 1 (PDK1), and mammalian target of rapamycin (mTOR). We found that PDGF-BB induced AKT binding to actin, and that Tβ4 prevented this effect. Tβ4 also prevented the activation of freshly isolated HSC cultured in the presence of Dulbecco's modified Eagle's medium or Dulbecco's minimal essential medium containing 10% fetal bovine serum. In conclusion, overall, our findings suggest that Tβ4 by sequestering actin prevents binding of AKT, thus inhibiting its phosphorylation. Therefore, Tβ4 has the potential to be an antifibrogenic agent.

Indexed as

ActinsBecaplerminBlotting, WesternCell MovementCell ProliferationCell SeparationCell TransdifferentiationFlow CytometryFluorescent Antibody TechniqueHepatic Stellate CellsHumansImmunoprecipitationLiver CirrhosisPhosphorylationPlatelet-Derived Growth FactorProtein BindingActinsBecaplerminPlatelet-Derived Growth FactorProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-sisThymosinThymosin beta(4)

Identifiers

PMID21514425
PMCPMC3081167
OpenAlexW2029695667

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.