Evidence map›Paper›PMID 15030515›Full record

ArticleClinical and experimental immunology2004

The membrane attack complex, C5b-9, up regulates collagen gene expression in renal tubular epithelial cells.

K Abe, K Li, S H Sacks, N S Sheerin

Open access · greenAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2004. 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
1.4field-weighted citation impact, top 19% 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, 51 citations in OpenAlex.

  1. Review
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  9. Review
  10. Review
  11. Article
  12. Complement activation in progressive renal disease.World journal of nephrology · 2015
    Review
  13. Inflammatory processes in renal fibrosis.Nature reviews. Nephrology · 2014
    Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. C3a mediates epithelial-to-mesenchymal transition in proteinuric nephropathy.Journal of the American Society of Nephrology : JASN · 2009
    Article
  19. Article
  20. Complement in glomerular injury.Seminars in immunopathology · 2007
    Review
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 2 institutions in 1 country.

K AbeDepartment of Nephrology and Transplantation, Guy's, King's and St Thomas' School of Medicine, Dentistry and Biomedical Science, King's College London, UK.
K Li
S H Sacks
N S Sheerin
King's College London · GBKing's College School · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Evidence suggesting a direct role for proteinuria in the pathogenesis of renal tubulointerstitial fibrosis is accumulating. However the mechanism by which proteinuria leads to injury is unknown. In proteinuric states complement proteins are filtered through the glomerulus and could contribute to the tubular damage. The aim of this study was to investigate the role of complement activation in the progression of interstitial fibrosis. To determine whether complement activation may be responsible for the pro-fibrotic response that occurs in the tubulointerstitial compartment we stimulated primary cultures of proximal tubular epithelial cells with membrane attack complex, C5b-9. This led to increased mRNA concentrations of both collagen type IV and its intracellular chaperone, Heat Shock Protein 47 (HSP47). To determine whether this occurred in vivo Adriamycin was used to induce proteinuria in female Balb/c mice. The expression of collagen type IV and HSP47 was increased in proteinuric mice compared to control mice. In proteinuric mouse kidney, C3 was deposited at sites of tubulointerstitial injury and there was a relationship between C3 deposition and immunochemical staining for collagen type IV and HSP47. In situ hybridization suggested that the renal tubular epithelium was actively expressing HSP47 mRNA and, by implication, excess collagen. These observations support the hypothesis that complement activation on tubular epithelial cells can directly increase the pro-fibrotic process associated with tubulointerstitial damage.

Indexed as

AlbuminuriaAnimalsCells, CulturedCollagenComplement Membrane Attack ComplexDoxorubicinEpithelial CellsFemaleHeat-Shock ProteinsHSP47 Heat-Shock ProteinsKidney TubulesMiceMice, Inbred BALB CNephritis, InterstitialReverse Transcriptase Polymerase Chain ReactionRNA, MessengerCollagenComplement Membrane Attack ComplexDoxorubicinHeat-Shock ProteinsHSP47 Heat-Shock ProteinsRNA, MessengerSerpinh1 protein, mouse

Identifiers

PMID15030515
PMCPMC1808988
OpenAlexW2044609989

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.