Evidence map›Paper›PMID 11021838›Full record

ArticleThe American journal of pathology2000

Glucose stimulation of transforming growth factor-beta bioactivity in mesangial cells is mediated by thrombospondin-1.

M H Poczatek, C Hugo, V Darley-Usmar, J E Murphy-Ullrich

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

44 citing papers in PubMed, 104 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Thrombospondin-1 CD47 Signalling: From Mechanisms to Medicine.International journal of molecular sciences · 2021
    Review
  6. Diabetic fibrosis.Biochimica et biophysica acta. Molecular basis of disease · 2021
    Review
  7. Article
  8. Article
  9. Blocking thrombospondin-1 signaling via CD47 mitigates renal interstitial fibrosis.Laboratory investigation; a journal of technical methods and pathology · 2020
    Article
  10. Article
  11. Article
  12. Thrombospondin 1 and Its Diverse Roles as a Regulator of Extracellular Matrix in Fibrotic Disease.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2019
    Review
  13. Article
  14. Thrombospondin-1 regulation of latent TGF-β activation: A therapeutic target for fibrotic disease.Matrix biology : journal of the International Society for Matrix Biology · 2018
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. The Thrombospondin1-TGF-β Pathway and Glaucoma.Journal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics · 2015
    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 3 institutions in 2 countries.

M H PoczatekDepartment of Pathology, Division of Molecular and Cellular Pathology, and The Cell Adhesion and Matrix Research Center, University of Alabama at Birmingham, Birmingham, Alabama, USA.
C Hugo
V Darley-Usmar
J E Murphy-Ullrich
University of Alabama at Birmingham · USFriedrich-Alexander-Universität Erlangen-Nürnberg · DEMatrix Research (United States) · US

Funding

REGULATION OF TGF-BETA ACTIVITY BY THROMBOSPONDINR01HL050061 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MURPHY-ULLRICH, JOANNE E · 1994 to 2004
$1.1M
THROMBOSPONDIN IN GLUCOSE-MEDIATED TGFB UPREGULATIONR01DK054624 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MURPHY-ULLRICH, JOANNE E · 1998 to 2001
$460k
NHLBI NIH HHS HL50061NHLBI NIH HHS R01 HL050061NIDDK NIH HHS DK54624
6 · The paper itself

Abstract

Glucose is a key factor in the development of diabetic complications, including diabetic nephropathy. The development of diabetic glomerulosclerosis is dependent on the fibrogenic growth factor, transforming growth factor-beta (TGF-beta). Previously we showed that thrombospondin-1 (TSP-1) activates latent TGF-beta both in vitro and in vivo. Activation occurs as the result of specific interactions of latent TGF-beta with TSP-1, which potentially alter the conformation of latent TGF-beta. As glucose also up-regulates TSP-1 expression, we hypothesized that the increased TGF-beta bioactivity observed in rat and human mesangial cells cultured with high glucose concentrations is the result of latent TGF-beta activation by autocrine TSP-1. Glucose-induced bioactivity of TGF-beta in mesangial cell cultures was reduced to basal levels by peptides from two different sequences that antagonize activation of latent TGF-beta by TSP, but not by the plasmin inhibitor, aprotinin. Furthermore, glucose-dependent stimulation of matrix protein synthesis was inhibited by these antagonist peptides. These studies demonstrate that glucose stimulation of TGF-beta activity and the resultant matrix protein synthesis are dependent on the action of autocrine TSP-1 to convert latent TGF-beta to its biologically active form. These data suggest that antagonists of TSP-dependent TGF-beta activation may be the basis of novel therapeutic approaches for ameliorating diabetic renal fibrosis.

Indexed as

AnimalsDose-Response Relationship, DrugExtracellular Matrix ProteinsGlomerular MesangiumGlucoseHumansKineticsMinkRatsThrombospondin 1Transforming Growth Factor betaUp-RegulationExtracellular Matrix ProteinsGlucoseThrombospondin 1Transforming Growth Factor beta

Identifiers

PMID11021838
PMCPMC1850177
OpenAlexW2013314129

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.