Evidence map›Paper›PMID 1939646›Full record

ArticleThe Journal of clinical investigation1991

Regulation of transforming growth factor-beta 1 gene expression by glucocorticoids in normal human T lymphocytes.

O AyanlarBatuman, A P Ferrero, A Diaz, S A Jimenez

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of clinical investigation, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

20 citing papers in PubMed, 134 citations in OpenAlex.

  1. Article
  2. Role of TGF-β1/SMADs signalling pathway in resveratrol-induced reduction of extracellular matrix deposition by dexamethasone-treated human trabecular meshwork cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2024
    Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Transplantation tolerance: fooling mother nature.Proceedings of the National Academy of Sciences of the United States of America · 1996
    Review
  15. Article
  16. 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

4 authors at 1 institution in 1 country.

O AyanlarBatumanCardeza Foundation for Hematologic Research, Jefferson Medical College, Thomas Jefferson University, Philadelphia, Pennsylvania 19107.
A P Ferrero
A Diaz
S A Jimenez
Thomas Jefferson University · US

Funding

MECHANISMS OF CUTANEOUS INJURY IN LUPUS ERYTHEMATOSUSR01AM019101 · AM · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI SONTHEIMER, RICHARD DENNIS · 1985 to 1985
–
LUNG FIBROSIS--MECHANISMS OF COLLAGEN GENE EXPRESSIONR01HL041214 · NHLBI · THOMAS JEFFERSON UNIVERSITY · PI JIMENEZ, SERGIO A · 1988 to 1992
–
NHLBI NIH HHS HL41214NIADDK NIH HHS AM 19101
6 · The paper itself

Abstract

Glucocorticoids (GC) modulate immune function in a number of ways, including suppression of T cell proliferation and other IL-2-mediated T cell functions. These inhibitory effects are similar to those induced by transforming growth factor-beta 1 (TGF-beta 1), a cytokine with potent T cell inhibiting activities. We examined the hypothesis that GC effects may be at least partially achieved through modulation of the expression of the TGF-beta 1 gene in activated T cells. Normal T cells were cultured with or without purified phytohemagglutinin (PHA-p) and 4 beta-phorbol 12-myristate 13-acetate (PMA) in the presence or absence of the synthetic GC, dexamethasone (100-200 micrograms/ml). The production of latent and active forms of TGF beta by these cells were analyzed by immunoblotting and bioassays. The steady-state levels of TGF-beta 1 mRNA were analyzed in total RNA from these cells by Northern hybridizations using a human TGF-beta 1 cDNA. The results showed that dexamethasone caused an increase in TGF beta production and a dose-dependent two to fourfold increase in TGF-beta 1 mRNA in activated as well as in unstimulated T cells, 1 h after exposure of the cultures to the steroid. The increase in TGF-beta 1 mRNA levels by dexamethasone was further potentiated two to threefold by cycloheximide, suggesting that the steroid effect may be due to inhibition of the synthesis of proteins that decrease TGF-beta 1 gene transcription or the stability of its transcripts. Finally, in vitro nuclear transcription studies indicated the dexamethasone effects on TGF-beta 1 gene expression to be largely transcriptional.

Indexed as

Cells, CulturedCycloheximideDexamethasoneGene Expression RegulationHumansLymphocyte ActivationT-LymphocytesTranscription, GeneticTransforming Growth Factor betaCycloheximideDexamethasoneTransforming Growth Factor beta

Identifiers

PMID1939646
PMCPMC295675
OpenAlexW2100745967

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.