Evidence map›Paper›PMID 20554619›Full record

ArticleInvestigative ophthalmology & visual science2011

The α7-nicotinic acetylcholine receptor and MMP-2/-9 pathway mediate the proangiogenic effect of nicotine in human retinal endothelial cells.

Aaron M Dom, Adam W Buckley, Kathleen C Brown, Richard D Egleton, Aileen J Marcelo, Nancy A Proper, Donald E Weller, Yashoni H Shah, Jamie K Lau, Piyali Dasgupta

Open access · bronzeAbstract readComparative Study
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 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

24 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
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  5. Review
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  7. Article
  8. Article
  9. Article
  10. Nicotine and vascular dysfunction.Acta physiologica (Oxford, England) · 2021
    Review
  11. Article
  12. Nicotine increased VEGF and MMP2 levels in the rat eye and kidney.Environmental science and pollution research international · 2019
    Article
  13. Article
  14. Article
  15. Endothelial CaInternational journal of molecular sciences · 2018
    Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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

10 authors at 2 institutions in 1 country.

Aaron M DomDepartment of Pharmacology, Physiology, and Toxicology, Joan C. Edwards School of Medicine, Marshall University, Huntington, West Virginia 25755, USA
Adam W Buckley
Kathleen C Brown
Richard D Egleton
Aileen J Marcelo
Nancy A Proper
Donald E Weller
Yashoni H Shah
Jamie K Lau
Piyali Dasgupta
Marshall University · USUniversity of Charleston · US

Funding

WVU &MU NEW FACULTY GRANTSP20RR016477 · NCRR · MARSHALL UNIVERSITY · PI RANKIN, GARY O · 2001 to 2011
$35.5M
Diabetes and Stroke: A Role for the Blood CNS BarriersR01DK065003 · NIDDK · UNIVERSITY OF ARIZONA · PI EGLETON, RICHARD DANIEL · 2004 to 2007
$1.1M
NCRR NIH HHS 3P20RR016477NCRR NIH HHS P20 RR016477NIDDK NIH HHS DK65003
6 · The paper itself

Abstract

purposeNicotine, the active component of cigarette smoke, has been found to stimulate angiogenesis in several experimental systems. In this study, the Matrigel duplex assay (Matrigel; BD Biosciences, Franklin Lakes, NJ) and the rat retinal explant assay were used to explore the molecular mechanisms underlying the proangiogenic effects of nicotine in endothelial cells.

methodsWestern blot analysis was performed to determine the nicotinic acetylcholine receptor (nAChR) subtypes expressed on primary human retinal microvascular endothelial cells (HRMECs). The angiogenic effect of nicotine in the retina was evaluated with the duplex assay. The results obtained from the assay were confirmed by the rat retinal explant angiogenesis assay. ELISAs were used to measure MMP-2, -9, and -13 levels in HRMEC culture supernatants. The role of α7-nAChRs in nicotine-induced angiogenesis was examined by siRNA techniques.

resultsNicotine-induced angiogenesis required nAChR function and was associated with the upregulation of MMP-2 and -9 in HRMECs. Specifically, α7-nAChRs mediated the stimulatory effects of nicotine on retinal angiogenesis and MMP levels. Treatment of HRMECs with α7-nAChR antagonists ablated nicotine-induced angiogenesis. The inhibitory actions of α7-nAChR antagonists correlated with the suppression of MMP-2 and -9 levels in HRMECs.

conclusionsThe α7-nAChR is vital for the proangiogenic activity of nicotine. The α7-nAChRs expressed on HRMECs upregulate levels of MMP-2 and -9, which stimulate retinal angiogenesis. The data also suggest that α7-nAChR antagonists could be useful agents for the therapy of angiogenesis-related retinal diseases.

Indexed as

alpha7 Nicotinic Acetylcholine ReceptorAnimalsBlotting, WesternCells, CulturedDisease Models, AnimalEndothelial CellsEndothelium, VascularEnzyme-Linked Immunosorbent AssayHumansMaleMatrix Metalloproteinase 2Matrix Metalloproteinase 9NicotineRatsRats, ZuckerReceptors, Nicotinicalpha7 Nicotinic Acetylcholine ReceptorChrna7 protein, humanChrna7 protein, ratMatrix Metalloproteinase 2Matrix Metalloproteinase 9NicotineReceptors, Nicotinic

Identifiers

PMID20554619
PMCPMC3175965
OpenAlexW1970352900

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.