Evidence map›Paper›PMID 26112010›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2015

Both MC1 and MC3 Receptors Provide Protection From Cerebral Ischemia-Reperfusion-Induced Neutrophil Recruitment.

Paul M Holloway, Pascal F Durrenberger, Marjan Trutschl, Urska Cvek, Dianne Cooper, A Wayne Orr, Mauro Perretti, Stephen J Getting, Felicity N E Gavins

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.1field-weighted citation impact, top 21% 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

18 citing papers in PubMed, 28 citations in OpenAlex.

  1. Trial
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  5. Regulating Neutrophil PAD4/NOX-Dependent Cerebrovasular Thromboinflammation.International journal of biological sciences · 2023
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  16. An atypical role for the myeloid receptor Mincle in central nervous system injury.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2017
    Article
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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

9 authors at 3 institutions in 2 countries.

Paul M HollowayFrom the Division of Brain Sciences, Imperial College London, London, United Kingdom (P.M.H., P.F.D., F.N.E.G.); LSU Shreveport, LA (M.T., U.C.); William Harvey Research Institute, Barts and The Royal London School of Medicine, London, United Kingdom (D.C., M.P.); Faculty of Science and Technology, University of Westminster, London, United Kingdom (S.J.G.); and LSU Health Science Center, Shreveport, LA (P.M.H., A.W.O., F.N.E.G.).
Pascal F DurrenbergerFrom the Division of Brain Sciences, Imperial College London, London, United Kingdom (P.M.H., P.F.D., F.N.E.G.); LSU Shreveport, LA (M.T., U.C.); William Harvey Research Institute, Barts and The Royal London School of Medicine, London, United Kingdom (D.C., M.P.); Faculty of Science and Technology, University of Westminster, London, United Kingdom (S.J.G.); and LSU Health Science Center, Shreveport, LA (P.M.H., A.W.O., F.N.E.G.).
Marjan TrutschlFrom the Division of Brain Sciences, Imperial College London, London, United Kingdom (P.M.H., P.F.D., F.N.E.G.); LSU Shreveport, LA (M.T., U.C.); William Harvey Research Institute, Barts and The Royal London School of Medicine, London, United Kingdom (D.C., M.P.); Faculty of Science and Technology, University of Westminster, London, United Kingdom (S.J.G.); and LSU Health Science Center, Shreveport, LA (P.M.H., A.W.O., F.N.E.G.).
Urska CvekFrom the Division of Brain Sciences, Imperial College London, London, United Kingdom (P.M.H., P.F.D., F.N.E.G.); LSU Shreveport, LA (M.T., U.C.); William Harvey Research Institute, Barts and The Royal London School of Medicine, London, United Kingdom (D.C., M.P.); Faculty of Science and Technology, University of Westminster, London, United Kingdom (S.J.G.); and LSU Health Science Center, Shreveport, LA (P.M.H., A.W.O., F.N.E.G.).
Dianne CooperFrom the Division of Brain Sciences, Imperial College London, London, United Kingdom (P.M.H., P.F.D., F.N.E.G.); LSU Shreveport, LA (M.T., U.C.); William Harvey Research Institute, Barts and The Royal London School of Medicine, London, United Kingdom (D.C., M.P.); Faculty of Science and Technology, University of Westminster, London, United Kingdom (S.J.G.); and LSU Health Science Center, Shreveport, LA (P.M.H., A.W.O., F.N.E.G.).
A Wayne OrrFrom the Division of Brain Sciences, Imperial College London, London, United Kingdom (P.M.H., P.F.D., F.N.E.G.); LSU Shreveport, LA (M.T., U.C.); William Harvey Research Institute, Barts and The Royal London School of Medicine, London, United Kingdom (D.C., M.P.); Faculty of Science and Technology, University of Westminster, London, United Kingdom (S.J.G.); and LSU Health Science Center, Shreveport, LA (P.M.H., A.W.O., F.N.E.G.).
Mauro PerrettiFrom the Division of Brain Sciences, Imperial College London, London, United Kingdom (P.M.H., P.F.D., F.N.E.G.); LSU Shreveport, LA (M.T., U.C.); William Harvey Research Institute, Barts and The Royal London School of Medicine, London, United Kingdom (D.C., M.P.); Faculty of Science and Technology, University of Westminster, London, United Kingdom (S.J.G.); and LSU Health Science Center, Shreveport, LA (P.M.H., A.W.O., F.N.E.G.).
Stephen J GettingFrom the Division of Brain Sciences, Imperial College London, London, United Kingdom (P.M.H., P.F.D., F.N.E.G.); LSU Shreveport, LA (M.T., U.C.); William Harvey Research Institute, Barts and The Royal London School of Medicine, London, United Kingdom (D.C., M.P.); Faculty of Science and Technology, University of Westminster, London, United Kingdom (S.J.G.); and LSU Health Science Center, Shreveport, LA (P.M.H., A.W.O., F.N.E.G.).
Felicity N E GavinsFrom the Division of Brain Sciences, Imperial College London, London, United Kingdom (P.M.H., P.F.D., F.N.E.G.); LSU Shreveport, LA (M.T., U.C.); William Harvey Research Institute, Barts and The Royal London School of Medicine, London, United Kingdom (D.C., M.P.); Faculty of Science and Technology, University of Westminster, London, United Kingdom (S.J.G.); and LSU Health Science Center, Shreveport, LA (P.M.H., A.W.O., F.N.E.G.). fgavin@lsuhsc.edu.
University of Westminster · GBWilliam Harvey Research Institute · GBLouisiana State University in Shreveport · US

Funding

COBRE Center for Molecular and Tumor VirologyP30GM110703 · NIGMS · LOUISIANA STATE UNIV HSC SHREVEPORT · PI SAPP, MARTIN · 2014 to 2018
$4.8M
British Heart Foundation FS/09/020/27184Medical Research Council MC_PC_12015NIGMS NIH HHS P30 GM110703NIGMS NIH HHS P30GM110703
6 · The paper itself

Abstract

objectiveNeutrophil recruitment is a key process in the pathogenesis of stroke, and may provide a valuable therapeutic target. Targeting the melanocortin (MC) receptors has previously shown to inhibit leukocyte recruitment in peripheral inflammation, however, it is not known whether treatments are effective in the unique cerebral microvascular environment. Here, we provide novel research highlighting the effects of the MC peptides on cerebral neutrophil recruitment, demonstrating important yet discrete roles for both MC1 and MC3. APPROACH AND

resultsUsing intravital microscopy, in 2 distinct murine models of cerebral ischemia-reperfusion (I/R) injury, we have investigated MC control for neutrophil recruitment. After global I/R, pharmacological treatments suppressed pathological neutrophil recruitment. MC1 selective treatment rapidly inhibited neutrophil recruitment while a nonselective MC agonist provided protection even when coadministered with an MC3/4 antagonist, suggesting the importance of early MC1 signaling. However, by 2-hour reperfusion, MC1-mediated effects were reduced, and MC3 anti-inflammatory circuits predominated. Mice bearing a nonfunctional MC1 displayed a transient exacerbation of neutrophil recruitment after global I/R, which diminished by 2 hours. However importantly, enhanced inflammatory responses in both MC1 mutant and MC3 (-/-) mice resulted in increased infarct size and poor functional outcome after focal I/R. Furthermore, we used an in vitro model of leukocyte recruitment to demonstrate these anti-inflammatory actions are also effective in human cells.

conclusionsThese studies reveal for the first time MC control for neutrophil recruitment in the unique pathophysiological context of cerebral I/R, while also demonstrating the potential therapeutic value of targeting multiple MCs in developing effective therapeutics.

Indexed as

Gene Expression RegulationAnimalsBrain IschemiaDisease Models, AnimalHumansMaleMelanocyte-Stimulating HormonesMiceNeutrophil InfiltrationReceptor, Melanocortin, Type 1Receptor, Melanocortin, Type 3Reperfusion InjuryRNA, MessengerMelanocyte-Stimulating HormonesReceptor, Melanocortin, Type 1Receptor, Melanocortin, Type 3RNA, MessengerSHU 9119inflammationleukocytemelanocortinsneutrophilstroke

Identifiers

PMID26112010
PMCPMC4552587
OpenAlexW1960087948

What OpenQuestion holds

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Registered trials

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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.