Evidence map›Paper›PMID 19487812›Full record

ArticleThe Journal of clinical investigation2009

The natriuretic peptide/guanylyl cyclase--a system functions as a stress-responsive regulator of angiogenesis in mice.

Michaela Kuhn, Katharina Völker, Kristine Schwarz, Javier Carbajo-Lozoya, Ulrich Flögel, Christoph Jacoby, Jörg Stypmann, Martin van Eickels, Stepan Gambaryan, Michael Hartmann and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

58 citing papers in PubMed, 105 citations in OpenAlex.

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  7. The Natriuretic Peptide System: A Single Entity, Pleiotropic Effects.International journal of molecular sciences · 2023
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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

14 authors at 6 institutions in 3 countries.

Michaela KuhnInstitute of Physiology, University of Würzburg, Würzburg, Germany. michaela.kuhn@mail.uni-wuerzburg.de
Katharina Völker
Kristine Schwarz
Javier Carbajo-Lozoya
Ulrich Flögel
Christoph Jacoby
Jörg Stypmann
Martin van Eickels
Stepan Gambaryan
Michael Hartmann
Matthias Werner
Thomas Wieland
Jürgen Schrader
Hideo A Baba
University of Würzburg · DEHeinrich Heine University Düsseldorf · DEHeidelberg University · DEChelsea and Westminster Hospital · GBInstitute of Evolutionary Physiology and Biochemistry · RUUniversity of Duisburg-Essen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiac atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) modulate blood pressure and volume by activation of the receptor guanylyl cyclase-A (GC-A) and subsequent intracellular cGMP formation. Here we report what we believe to be a novel function of these peptides as paracrine regulators of vascular regeneration. In mice with systemic deletion of the GC-A gene, vascular regeneration in response to critical hind limb ischemia was severely impaired. Similar attenuation of ischemic angiogenesis was observed in mice with conditional, endothelial cell-restricted GC-A deletion (here termed EC GC-A KO mice). In contrast, smooth muscle cell-restricted GC-A ablation did not affect ischemic neovascularization. Immunohistochemistry and RT-PCR revealed BNP expression in activated satellite cells within the ischemic muscle, suggesting that local BNP elicits protective endothelial effects. Since within the heart, BNP is mainly induced in cardiomyocytes by mechanical load, we investigated whether the natriuretic peptide/GC-A system also regulates angiogenesis accompanying load-induced cardiac hypertrophy. EC GC-A KO hearts showed diminished angiogenesis, mild fibrosis, and diastolic dysfunction. In vitro BNP/GC-A stimulated proliferation and migration of cultured microvascular endothelia by activating cGMP-dependent protein kinase I and phosphorylating vasodilator-stimulated phosphoprotein and p38 MAPK. We therefore conclude that BNP, produced by activated satellite cells within ischemic skeletal muscle or by cardiomyocytes in response to pressure load, regulates the regeneration of neighboring endothelia via GC-A. This paracrine communication might be critically involved in coordinating muscle regeneration/hypertrophy and angiogenesis.

Indexed as

Neovascularization, PhysiologicAnimalsCardiomegalyCell Adhesion MoleculesCell MovementCell ProliferationCells, CulturedCoronary VesselsEndothelial CellsFemaleGuanylate CyclaseHindlimbIschemiaMaleMiceMicrofilament ProteinsCell Adhesion MoleculesGuanylate CyclaseMicrofilament ProteinsNatriuretic Peptide, Brainp38 Mitogen-Activated Protein KinasesPhosphoproteinsRNA, MessengerVasodilator-Stimulated Phosphoprotein

Identifiers

PMID19487812
PMCPMC2701863
OpenAlexW3023914306

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.