Evidence map›Paper›PMID 31729436›Full record

ArticleScientific reports2019

Requirement of β1 integrin for endothelium-dependent vasodilation and collateral formation in hindlimb ischemia.

Carina Henning, Anna Branopolski, Dominik Schuler, Dimitrios Dimitroulis, Patrik Huelsemann, Christopher Nicolaus, Roberto Sansone, Jelle Ludolf Postma, Daniel Eberhard, Ferdinand Le Noble and 3 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

11 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Review
  3. Endothelial β1-integrins are necessary for microvascular function and glucose uptake.American journal of physiology. Endocrinology and metabolism · 2024
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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

13 authors at 4 institutions in 2 countries.

Carina HenningInstitute of Metabolic Physiology, Heinrich Heine University, Duesseldorf, Germany.
Anna BranopolskiInstitute of Metabolic Physiology, Heinrich Heine University, Duesseldorf, Germany.
Dominik SchulerDivision of Cardiology, Pulmonology, and Vascular Medicine, Medical Faculty, University Duesseldorf, Duesseldorf, Germany.
Dimitrios DimitroulisDivision of Cardiology, Pulmonology, and Vascular Medicine, Medical Faculty, University Duesseldorf, Duesseldorf, Germany.
Patrik HuelsemannDivision of Cardiology, Pulmonology, and Vascular Medicine, Medical Faculty, University Duesseldorf, Duesseldorf, Germany.
Christopher NicolausDivision of Cardiology, Pulmonology, and Vascular Medicine, Medical Faculty, University Duesseldorf, Duesseldorf, Germany.
Roberto SansoneDivision of Cardiology, Pulmonology, and Vascular Medicine, Medical Faculty, University Duesseldorf, Duesseldorf, Germany.
Jelle Ludolf PostmaCenter for Advanced Imaging, Heinrich Heine University Duesseldorf, Duesseldorf, Germany.ORCID http://orcid.org/0000-0001-5772-5764
Daniel EberhardInstitute of Metabolic Physiology, Heinrich Heine University, Duesseldorf, Germany.
Ferdinand Le NobleInstitute for Zoology, Karlsruhe Institute of Technology, Karlsruhe, Germany.
Malte KelmDivision of Cardiology, Pulmonology, and Vascular Medicine, Medical Faculty, University Duesseldorf, Duesseldorf, Germany.
Eckhard LammertInstitute of Metabolic Physiology, Heinrich Heine University, Duesseldorf, Germany. lammert@hhu.de.
Christian HeissDivision of Cardiology, Pulmonology, and Vascular Medicine, Medical Faculty, University Duesseldorf, Duesseldorf, Germany. c.heiss@surrey.ac.uk.ORCID http://orcid.org/0000-0002-3212-8995
Heinrich Heine University Düsseldorf · DEDeutsches Diabetes-Zentrum e.V. · DEEast Surrey Hospital · GBKarlsruhe Institute of Technology · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

An acute increase in blood flow triggers flow-mediated dilation (FMD), which is mainly mediated by endothelial nitric oxide synthase (eNOS). A long-term increase in blood flow chronically enlarges the arterial lumen, a process called arteriogenesis. In several common human diseases, these processes are disrupted for as yet unknown reasons. Here, we asked whether β1 integrin, a mechanosensory protein in endothelial cells, is required for FMD and arteriogenesis in the ischemic hindlimb. Permanent ligation of the femoral artery in C57BL/6 J mice enlarged pre-existing collateral arteries and increased numbers of arterioles in the thigh. In the lower leg, the numbers of capillaries increased. Notably, injection of β1 integrin-blocking antibody or tamoxifen-induced endothelial cell-specific deletion of the gene for β1 integrin (Itgb1) inhibited both arteriogenesis and angiogenesis. Using high frequency ultrasound, we demonstrated that β1 integrin-blocking antibody or endothelial cell-specific depletion of β1 integrin attenuated FMD of the femoral artery, and blocking of β1 integrin function did not further decrease FMD in eNOS-deficient mice. Our data suggest that endothelial β1 integrin is required for both acute and chronic widening of the arterial lumen in response to hindlimb ischemia, potentially via functional interaction with eNOS.

Indexed as

VasodilationAnimalsCollateral CirculationDisease Models, AnimalEndothelial CellsEndothelium, VascularGene Knockout TechniquesHindlimbHumansIntegrin beta1IschemiaMiceMice, KnockoutNeovascularization, PhysiologicNitric Oxide Synthase Type IIIProtein BindingIntegrin beta1Nitric Oxide Synthase Type III

Identifiers

PMID31729436
PMCPMC6858366
OpenAlexW2983970802

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.