Evidence map›Paper›PMID 27239731›Full record

ArticleLaboratory investigation; a journal of technical methods and pathology2016

Arginase inhibition attenuates arteriogenesis and interferes with M2 macrophage accumulation.

Manuel Lasch, Amelia Caballero-Martinez, Kerstin Troidl, Irmengard Schloegl, Thomas Lautz, Elisabeth Deindl

Abstract read
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In one paragraph

Article in Laboratory investigation; a journal of technical methods and pathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.2field-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

15 citing papers in PubMed, 14 citations in OpenAlex.

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  15. Arteriogenesis in murine adipose tissue is contingent on CD68Microcirculation (New York, N.Y. : 1994) · 2017
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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 2 institutions in 1 country.

Manuel LaschWalter-Brendel-Centre of Experimental Medicine, LMU Munich, Munich, Germany.
Amelia Caballero-MartinezWalter-Brendel-Centre of Experimental Medicine, LMU Munich, Munich, Germany.
Kerstin TroidlMax-Planck-Institute for Heart and Lung Research, Bad Nauheim, Germany.
Irmengard SchloeglWalter-Brendel-Centre of Experimental Medicine, LMU Munich, Munich, Germany.
Thomas LautzWalter-Brendel-Centre of Experimental Medicine, LMU Munich, Munich, Germany.
Elisabeth DeindlWalter-Brendel-Centre of Experimental Medicine, LMU Munich, Munich, Germany.
Ludwig-Maximilians-Universität München · DEGoethe University Frankfurt · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

l-Arginine is the common substrate for nitric oxide synthases (NOS) and arginase. Whereas the contribution of NOS to collateral artery growth (arteriogenesis) has been demonstrated, the functional role of arginase remains to be elucidated and was topic of the present study. Arteriogenesis was induced in mice by ligation of the femoral artery. Laser Doppler perfusion measurements demonstrated a significant reduction in arteriogenesis in mice treated with the arginase inhibitor nor-NOHA (N(ω)-hydroxy-nor-arginine). Accompanying in vitro results on murine primary arterial endothelial cells and smooth muscle cells revealed that nor-NOHA treatment interfered with cell proliferation and resulted in increased nitrate/nitrite levels, indicative for increased NO production. Immuno-histological analyses on tissue samples demonstrated that nor-NOHA administration caused a significant reduction in M2 macrophage accumulation around growing collateral arteries. Gene expression studies on isolated growing collaterals evidenced that nor-NOHA treatment abolished the differential expression of Icam1 (intercellular adhesion molecule 1). From our data we conclude that arginase activity is essential for arteriogenesis by promoting perivascular M2 macrophage accumulation as well as arterial cell proliferation.

Indexed as

AnimalsArginaseArginineArteriesCell ProliferationCells, CulturedCollateral CirculationEndothelial CellsEnzyme InhibitorsGene ExpressionIntercellular Adhesion Molecule-1MacrophagesMaleMiceMice, Inbred C57BLMyocytes, Smooth MuscleArginaseArginineEnzyme InhibitorsIcam1 protein, mouseIntercellular Adhesion Molecule-1Nitric OxideN(omega)-hydroxynorarginine

Identifiers

PMID27239731
OpenAlexW2397250407

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.