Evidence map›Paper›PMID 18822317›Full record

ArticleImmunology letters2008

Pathogenic anti-DNA antibodies modulate gene expression in mesangial cells: involvement of HMGB1 in anti-DNA antibody-induced renal injury.

Xiaoping Qing, Milena Pitashny, David B Thomas, Franck J Barrat, Mark P Hogarth, Chaim Putterman

Open access · greenAbstract read
In one paragraph

Article in Immunology letters, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.2field-weighted citation impact, top 9% 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

39 citing papers in PubMed, 79 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Targeting HMGB1: A Potential Therapeutic Strategy for Chronic Kidney Disease.International journal of biological sciences · 2023
    Review
  6. Mesangial cell: A hub in lupus nephritis.Frontiers in immunology · 2022
    Review
  7. Article
  8. Article
  9. Review
  10. Toll-Like Receptor as a Potential Biomarker in Renal Diseases.International journal of molecular sciences · 2020
    Review
  11. HMGB1 in Systemic Lupus Erythematosus.Frontiers in immunology · 2020
    Review
  12. Article
  13. Toll-like receptors in lupus nephritis.Journal of biomedical science · 2018
    Review
  14. Review
  15. Article
  16. Article
  17. Review
  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

6 authors at 4 institutions in 3 countries.

Xiaoping QingThe Department of Microbiology & Immunology, Albert Einstein College of Medicine, Bronx, NY, USA.
Milena Pitashny
David B Thomas
Franck J Barrat
Mark P Hogarth
Chaim Putterman
Albert Einstein College of Medicine · USYeshiva University · USDynavax Technologies (Germany) · DEUniversity of Melbourne · AU

Funding

Studies of systemic lupus erythematosusP01AI051392 · NIAID · YESHIVA UNIVERSITY · PI DIAMOND, BETTY · 2002 to 2006
$5.1M
The Renal Pathogenicity of anti-DNA AntibodiesR01AR048692 · NIAMS · YESHIVA UNIVERSITY · PI PUTTERMAN, CHAIM · 2002 to 2013
$4.0M
The Renal Pathogenicity of Anti-DNA AntibodiesR56AR048692 · NIAMS · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI PUTTERMAN, CHAIM · 2008 to 2008
$365k
NIAID NIH HHS P01 AI051392NIAID NIH HHS P01 AI51392NIAMS NIH HHS R01 AR048692NIAMS NIH HHS R01 AR48692NIAMS NIH HHS R56 AR048692
6 · The paper itself

Abstract

Although anti-DNA antibodies have been decisively linked to the pathogenesis of lupus nephritis, the mechanisms have not been conclusively determined. Recently, we reported that anti-DNA antibodies may contribute to kidney damage by upregulation of proinflammatory genes in mesangial cells (MC), a process involving both Fc receptor-dependent and independent pathways. In investigating the mechanism by which pathogenic anti-DNA antibodies modulate gene expression in MC, we found that the pathogenic anti-DNA antibody 1A3F bound to high mobility group binding protein 1 (HMGB1), an endogenous ligand for TLR2/4 and RAGE (receptor for advanced glycation end products). Interestingly, HMGB1 treatment of MC induced a similar pattern of genes as stimulation with 1A3F. Furthermore, HMGB1 and 1A3F exhibited a synergistic proinflammatory effect in the kidney, where increased expression of HMGB1 was found in lupus patients but not in patients with other types of renal disease. TLR2/Fc and RAGE/Fc inhibited the proinflammatory effects of 1A3F on MC. Finally, we found enhanced susceptibility of lupus prone MRL-lpr/lpr (MRL/lpr) as compared to normal BALB/c derived MC to pathogenic anti-DNA antibody and LPS stimulation (in particular enhanced chemokine synthesis), in addition to significantly increased expression of TLR4. Our results suggest that gene upregulation in MC induced by nephritogenic anti-DNA antibodies is TLR2/4 and RAGE-dependent. Finally, HMGB1 may act as a proinflammatory mediator in antibody-induced kidney damage in systemic lupus erythematosus (SLE).

Indexed as

AnimalsAntibodies, AntinuclearDown-RegulationFemaleGene ExpressionHMGB1 ProteinHumansLupus Erythematosus, SystemicLupus NephritisMesangial CellsMiceMice, Inbred BALB CMice, Inbred MRL lprMitogen-Activated Protein KinasesMyeloid Differentiation Factor 88Toll-Like Receptor 2Antibodies, AntinuclearHMGB1 ProteinMitogen-Activated Protein KinasesMok protein, mouseMyd88 protein, mouseMyeloid Differentiation Factor 88Toll-Like Receptor 2Toll-Like Receptor 4

Identifiers

PMID18822317
PMCPMC2677706
OpenAlexW1969520387

What OpenQuestion holds

Textmetadata
LicenceTDM
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.