Evidence map›Paper›PMID 21345995›Full record

ArticleInvestigative ophthalmology & visual science2011

Biliverdin Rescues the HO-2 Null Mouse Phenotype of Unresolved Chronic Inflammation Following Corneal Epithelial Injury.

Lars Bellner, Jesse Wolstein, Kiran A Patil, Michael W Dunn, Michal Laniado-Schwartzman

Open access · bronzeAbstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing 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

28 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Immune challenges decrease biliverdin concentration in the spleen of northern Bobwhite quail, Colinus virginianus.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2018
    Article
  9. Article
  10. Heme Oxygenase 1 as a Therapeutic Target in Acute Kidney Injury.American journal of kidney diseases : the official journal of the National Kidney Foundation · 2017
    Review
  11. Article
  12. Article
  13. Review
  14. Rv2074 is a novel F420 H2 -dependent biliverdin reductase in Mycobacterium tuberculosis.Protein science : a publication of the Protein Society · 2016
    Article
  15. Article
  16. Heme oxygenase-2 deletion impairs macrophage function: implication in wound healing.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015
    Article
  17. Article
  18. Article
  19. Review
  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

5 authors at 1 institution in 1 country.

Lars BellnerDepartments of Pharmacology, New York Medical College, Valhalla, New York 10595, USA.
Jesse Wolstein
Kiran A Patil
Michael W Dunn
Michal Laniado-Schwartzman
New York Medical College · US

Funding

CORNEAL ARACHIDONATE METABOLITES VIA CYTOCHROME P450R01EY006513 · NEI · NEW YORK MEDICAL COLLEGE · PI SCHWARTZMAN, MICHAL LANIADO · 1987 to 2010
$4.2M
NEI NIH HHS EY06513NEI NIH HHS R01 EY006513
6 · The paper itself

Abstract

PURPOSE. The heme oxygenase system (HO-1 and HO-2) represents an intrinsic cytoprotective and anti-inflammatory pathway based on its ability to modulate leukocyte migration and to inhibit the expression of inflammatory cytokines and proteins by its products biliverdin/bilirubin and carbon monoxide. Corneal injury in HO-2 null mice leads to impaired healing and chronic inflammatory complications, including ulceration and neovascularization. The authors examined whether topically administered biliverdin can counteract the effects of HO deficiency in a corneal epithelial injury model. METHODS. HO-2 null mice were treated with biliverdin 1 hour before epithelial injury and twice a day thereafter. Reepithelialization and neovascularization were assessed by fluorescein staining and vital microscopy, respectively, and were quantified by image analysis. Inflammation was quantified by histology and Gr-1-specific immunofluorescence, and oxidative stress was assessed by DHE fluorescence. RESULTS. Treatment with biliverdin accelerated wound closure, inhibited neovascularization and reduced epithelial defects. It also reduced inflammation, as evidenced by a reduction in the appearance of inflammatory cells and the expression levels of inflammatory and oxidant proteins, including KC and NOXs. CONCLUSIONS. The results clearly show that biliverdin, directly or through its metabolism to bilirubin by biliverdin reductase-the expression of which is increased after injury-rescues the aberrant inflammatory phenotype, further underscoring the importance of the HO system in the cornea for the execution of an ordered inflammatory and reparative response.

Indexed as

Administration, TopicalAnimalsBiliverdineChemokinesChronic DiseaseCorneal NeovascularizationCorneal UlcerEnzyme-Linked Immunosorbent AssayEpithelium, CornealFluorescent Antibody Technique, IndirectHeme Oxygenase (Decyclizing)MiceMice, Inbred C57BLMice, KnockoutMicroscopy, FluorescenceOxidative StressBiliverdineChemokinesheme oxygenase-2Heme Oxygenase (Decyclizing)

Identifiers

PMID21345995
PMCPMC3109026
OpenAlexW1984445105

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.