Evidence map›Paper›PMID 1361494›Full record

ArticleThe Journal of clinical investigation1992

Rat glomerular mesangial cells synthesize basic fibroblast growth factor. Release, upregulated synthesis, and mitogenicity in mesangial proliferative glomerulonephritis.

J Floege, E Eng, V Lindner, C E Alpers, B A Young, M A Reidy, R J Johnson

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

27 citing papers in PubMed, 136 citations in OpenAlex.

  1. Article
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  4. Review
  5. Article
  6. Peritoneal damage by peritoneal dialysis solutions.Clinical and experimental nephrology · 2008
    Review
  7. Article
  8. Article
  9. A 20-year history of childhood HIV-associated nephropathy.Pediatric nephrology (Berlin, Germany) · 2004
    Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
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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 2 institutions in 1 country.

J FloegeDepartment of Medicine, University of Washington Medical Center, Seattle 98195.
E Eng
V Lindner
C E Alpers
B A Young
M A Reidy
R J Johnson
University of Washington · USUniversity of Washington Medical Center · US

Funding

PLATELETS IN IMMUNE GLOMERULAR INJURYR01DK043422 · NIDDK · UNIVERSITY OF WASHINGTON · PI JOHNSON, RICHARD JOSEPH · 1991 to 1999
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MYELOPEROXIDASE-H202-HALIDE SYSTEM IN GLOMERULAR INJURYR29DK039068 · NIDDK · UNIVERSITY OF WASHINGTON · PI JOHNSON, RICHARD JOSEPH · 1987 to 1991
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MESANGIAL RESPONSE TO INJURYR55DK043422 · NIDDK · UNIVERSITY OF WASHINGTON · PI JOHNSON, RICHARD JOSEPH · 1996 to 1996
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NHLBI NIH HHS HL-03174NIDDK NIH HHS DK-39068NIDDK NIH HHS DK-43422
6 · The paper itself

Abstract

Mesangial injury and cell proliferation are frequent findings in various glomerular diseases in man. Previous studies have demonstrated that basic fibroblast growth factor (bFGF) is a potent mesangial cell mitogen in vitro. To further elucidate the role of bFGF in rat mesangial cell (RMC) proliferation, we examined whether RMC synthesize bFGF in vitro and whether bFGF is involved in mesangial proliferation in vivo. Cultured RMC expressed bFGF protein (23, 21.5, and 18 kD forms) and bFGF mRNA, and released biologically active bFGF into the culture medium after antibody- and complement-mediated injury. Normal rat glomeruli in vivo contained no detectable bFGF mRNA, but bFGF protein (23 and 21.5 kD) could be demonstrated, which immunolocalized to the mesangium. Glomerular bFGF decreased markedly during the acute phase of glomerulonephritis induced by anti-Thy 1.1 antibody, compatible with mesangial bFGF release after complement-mediated mesangiolysis. During the subsequent mesangial proliferative phase, glomerular bFGF protein and mRNA increased above normal. Intrarenal infusion of heparin did not affect the bFGF immunostaining of glomeruli at this stage, indicating a predominantly intracellular localization of the bFGF. The capability of bFGF to mediate proliferation in the anti-Thy 1.1 model was further supported by experiments in which intravenous bFGF given 24 h after a subnephritogenic dose of anti-Thy 1.1 antibody led to a 4.9- to 5.1-fold increase in glomerular cell proliferation (with > 60% of the cells identified as mesangial cells by double immunolabeling). No such increase was observed in normal rats injected with bFGF. These data show that mesangial cells produce and release bFGF after injury and that bFGF is mitogenic for injured mesangial cells in vivo. Release of mesangial cell bFGF thus may be an important mechanism involved in the initiation of mesangial cell proliferation in vivo.

Indexed as

AnimalsAntibodies, MonoclonalAntigens, SurfaceBlotting, WesternCell DivisionCells, CulturedFibroblast Growth Factor 2Fluorescent Antibody TechniqueGene ExpressionGlomerular MesangiumGlomerulonephritis, MembranoproliferativeMembrane GlycoproteinsRatsRats, WistarRNA, MessengerThy-1 AntigensAntibodies, MonoclonalAntigens, SurfaceFibroblast Growth Factor 2Membrane GlycoproteinsRNA, MessengerThy-1 Antigens

Identifiers

PMID1361494
PMCPMC443391
OpenAlexW1978686331

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.