Evidence map›Paper›PMID 18042040›Full record

ArticleThe Biochemical journal2008

Hepcidin expression in mouse retina and its regulation via lipopolysaccharide/Toll-like receptor-4 pathway independent of Hfe.

Jaya P Gnana-Prakasam, Pamela M Martin, Barbara A Mysona, Penny Roon, Sylvia B Smith, Vadivel Ganapathy

Open access · greenAbstract read
In one paragraph

Article in The Biochemical journal, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
3.9field-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

61 citing papers in PubMed, 88 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Hepcidin and Tissue-Specific Iron Regulatory Networks.Advances in experimental medicine and biology · 2025
    Review
  6. Article
  7. Iron chelators: as therapeutic agents in diseases.Annals of medicine and surgery (2012) · 2024
    Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Retinal Degeneration and Alzheimer's Disease: An Evolving Link.International journal of molecular sciences · 2020
    Review
  17. Review
  18. Article
  19. Article
  20. Article

1 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Jaya P Gnana-PrakasamDepartment of Biochemistry and Molecular Biology, Medical College of Georgia, Augusta, GA 30912, USA.
Pamela M Martin
Barbara A Mysona
Penny Roon
Sylvia B Smith
Vadivel Ganapathy
Augusta University · US

Funding

Role of homocysteine in retinal diseaseR01EY012830 · NEI · MEDICAL COLLEGE OF GEORGIA (MCG) · PI SMITH, SYLVIA B. · 2000 to 2016
$4.4M
NEI NIH HHS R01 EY012830
6 · The paper itself

Abstract

Hepcidin is a hormone central to the regulation of iron homeostasis in the body. It is believed to be produced exclusively by the liver. Ferroportin, an iron exporter, is the receptor for hepcidin. This transporter/receptor is expressed in Müller cells, photoreceptor cells and the RPE (retinal pigment epithelium) within the retina. Since the retina is protected by the retinal-blood barriers, we asked whether ferroportin in the retina is regulated by hepcidin in the circulation or whether the retina produces hepcidin for regulation of its own iron homeostasis. Here we show that hepcidin is expressed robustly in Müller cells, photoreceptor cells and RPE cells, closely resembling the expression pattern of ferroportin. We also show that bacterial LPS (lipopolysaccharide) is a regulator of hepcidin expression in Müller cells and the RPE, both in vitro and in vivo, and that the regulation occurs at the transcriptional level. The action of LPS on hepcidin expression is mediated by the TLR4 (Toll-like receptor-4). The upregulation of hepcidin by LPS occurs independent of Hfe (human leukocyte antigen-like protein involved in Fe homeostasis). The increase in hepcidin levels in retinal cells in response to LPS treatment is associated with a decrease in ferroportin levels. The LPS-induced upregulation of hepcidin and consequent down-regulation of ferroportin is associated with increased oxidative stress and apoptosis within the retina in vivo. We conclude that retinal iron homeostasis may be regulated in an autonomous manner by hepcidin generated within the retina and that chronic bacterial infection/inflammation of the retina may disrupt iron homeostasis and retinal function.

Indexed as

Histocompatibility Antigens Class IMembrane ProteinsAnimalsAntimicrobial Cationic PeptidesApoptosisCation Transport ProteinsFerroportinGene Expression RegulationHemochromatosis ProteinHepcidinsHomeostasisIronLipopolysaccharidesMiceOxidative StressRetinaAntimicrobial Cationic PeptidesCation Transport ProteinsFerroportinHAMP protein, humanHamp protein, mouseHemochromatosis ProteinHepcidinsHfe protein, mouseHistocompatibility Antigens Class IIronLipopolysaccharidesMembrane ProteinsTlr4 protein, mouseToll-Like Receptor 4

Identifiers

PMID18042040
PMCPMC3731152
OpenAlexW1984109834

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.