Evidence map›Paper›PMID 21515678›Full record

ArticleThe Journal of biological chemistry2011

Relationship between complement membrane attack complex, chemokine (C-C motif) ligand 2 (CCL2) and vascular endothelial growth factor in mouse model of laser-induced choroidal neovascularization.

Juan Liu, Purushottam Jha, Valeriy V Lyzogubov, Ruslana G Tytarenko, Nalini S Bora, Puran S Bora

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 7% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. The Role of Complement Dysregulation in Glaucoma.International journal of molecular sciences · 2024
    Review
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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

6 authors at 1 institution in 1 country.

Juan LiuDepartment of Ophthalmology, University of Arkansas for Medical Sciences, Little Rock, Arizona 72205, USA.
Purushottam Jha
Valeriy V Lyzogubov
Ruslana G Tytarenko
Nalini S Bora
Puran S Bora
University of Arkansas for Medical Sciences · US

Funding

Complement System and Choroidal NeovascularizationR01EY014623 · NEI · UNIV OF ARKANSAS FOR MED SCIS · PI BORA, PURAN S · 2003 to 2011
$3.2M
Complement System and Idiopathic Anterior UveitisR01EY018812 · NEI · UNIV OF ARKANSAS FOR MED SCIS · PI BORA, NALINI S. · 2009 to 2011
$1.1M
NEI NIH HHS EY014623NEI NIH HHS EY018812NEI NIH HHS R01 EY014623NEI NIH HHS R01 EY018812
6 · The paper itself

Abstract

The present study investigated the interactions among the complement membrane attack complex (MAC), CCL2, and VEGF that occur in vivo during the development of choroidal neovascularization (CNV). We first investigated the sequential expression of MAC, CCL2, and VEGF during laser-induced CNV in C57BL/6 mice. Increased MAC deposition was detected at 1 h, CCL2 increased at 3 h, and VEGF was up-regulated at day 3 post-laser treatment. These results suggested that during laser-induced CNV, MAC, CCL2 and VEGF are formed and/or expressed in the following order: MAC → CCL2 → VEGF. To determine the cross-talk between MAC, CCL2, and VEGF during laser-induced CNV, neutralizing antibodies were injected both systemically and locally to block the bioactivity of each molecule. Blocking MAC formation inhibited CCL2 and VEGF expression and also limited CNV formation, whereas neutralization of CCL2 bioactivity did not affect MAC deposition; however, it reduced VEGF expression and CNV formation. When bioactivity of VEGF was blocked, CNV formation was significantly inhibited, but MAC deposition was not affected. Together, our results demonstrate that MAC is an upstream mediator and effect of MAC on the development of laser-induced CNV can be attributed to its direct effect on VEGF as well as its effect on VEGF that is mediated by CCL2. Understanding the interplay between immune mediators is critical to gain insight into the pathogenesis of CNV.

Indexed as

Gene Expression RegulationAnimalsAntibodies, NeutralizingChemokine CCL2Choroidal NeovascularizationComplement Membrane Attack ComplexDisease Models, AnimalLasersMiceTime FactorsVascular Endothelial Growth Factor AAntibodies, NeutralizingCcl2 protein, mouseChemokine CCL2Complement Membrane Attack ComplexVascular Endothelial Growth Factor Avascular endothelial growth factor A, mouse

Identifiers

PMID21515678
PMCPMC3121483
OpenAlexW1968327904

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.