Evidence map›Paper›PMID 28233474›Full record

ArticleStem cells translational medicine2017

Induced Pluripotent Stem Cell-Derived Endothelial Cells Overexpressing Interleukin-8 Receptors A/B and/or C-C Chemokine Receptors 2/5 Inhibit Vascular Injury Response.

Samantha Giordano, Xiangmin Zhao, Yiu-Fai Chen, Silvio H Litovsky, Fadi G Hage, Tim M Townes, Chiao-Wang Sun, Li-Chen Wu, Suzanne Oparil, Dongqi Xing

Open access · goldAbstract read
In one paragraph

Article in Stem cells translational medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.7field-weighted citation impact, top 28% 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

6 citing papers in PubMed, 7 citations in OpenAlex.

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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

10 authors at 1 institution in 1 country.

Samantha GiordanoVascular Biology and Hypertension Program, Division of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Xiangmin ZhaoVascular Biology and Hypertension Program, Division of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Yiu-Fai ChenVascular Biology and Hypertension Program, Division of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Silvio H LitovskyDivision of Anatomic Pathology, Department of Pathology, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Fadi G HageVascular Biology and Hypertension Program, Division of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Tim M TownesDepartment of Biochemistry and Molecular Genetics, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Chiao-Wang SunDepartment of Biochemistry and Molecular Genetics, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Li-Chen WuDepartment of Biochemistry and Molecular Genetics, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Suzanne OparilVascular Biology and Hypertension Program, Division of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Dongqi XingVascular Biology and Hypertension Program, Division of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA.
University of Alabama at Birmingham · US

Funding

University of Alabama at Birmingham's Diabetes Research CenterP30DK079626 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Kirk Michael Habegger · 2013 to 2026
$19.5M
MECHANISMS OF HYPERTENSION AND CARDIOVASCULAR DISEASEST32HL007457 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Martin E Young · 1985 to 2026
$8.6M
O-GlyNAcylation: Novel Mechanism of Estrogen-Induced VasoprotectionR01HL087980 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI OPARIL, SUZANNE · 2009 to 2012
$1.4M
Targeted Delivery of iPS-Endothelial Cells for the Repair of Cardiovascular InjurR01HL116727 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CHEN, YIU-FAI · 2013 to 2016
$1.4M
Targeted Cell Therapy for Acute Lung InjuryR56HL128285 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI XING, DONGQI · 2016 to 2016
$368k
Estrogen Effects on Vascular Inflammation are Age and Hormone-Status DependentI01BX001431 · VA · BIRMINGHAM VA MEDICAL CENTER · PI HAGE, FADI · 2013 to 2016
–
BLRD VA I01 BX001431NHLBI NIH HHS R01 HL087980NHLBI NIH HHS R01 HL116727NHLBI NIH HHS R56 HL128285NHLBI NIH HHS T32 HL007457NIDDK NIH HHS P30 DK079626
6 · The paper itself

Abstract

Recruitment of neutrophils and monocytes/macrophages to the site of vascular injury is mediated by binding of chemoattractants to interleukin (IL) 8 receptors RA and RB (IL8RA/B) C-C chemokine receptors (CCR) 2 and 5 expressed on neutrophil and monocyte/macrophage membranes. Endothelial cells (ECs) derived from rat-induced pluripotent stem cells (RiPS) were transduced with adenovirus containing cDNA of IL8RA/B and/or CCR2/5. We hypothesized that RiPS-ECs overexpressing IL8RA/B (RiPS-IL8RA/B-ECs), CCR2/5 (RiPS-CCR2/5-ECs), or both receptors (RiPS-IL8RA/B+CCR2/5-ECs) will inhibit inflammatory responses and neointima formation in balloon-injured rat carotid artery. Twelve-week-old male Sprague-Dawley rats underwent balloon injury of the right carotid artery and intravenous infusion of (a) saline vehicle, (b) control RiPS-Null-ECs (ECs transduced with empty virus), (c) RiPS-IL8RA/B-ECs, (d) RiPS-CCR2/5-ECs, or (e) RiPS-IL8RA/B+CCR2/5-ECs. Inflammatory mediator expression and leukocyte infiltration were measured in injured and uninjured arteries at 24 hours postinjury by enzyme-linked immunosorbent assay (ELISA) and immunohistochemistry, respectively. Neointima formation was assessed at 14 days postinjury. RiPS-ECs expressing the IL8RA/B or CCR2/5 homing device targeted the injured arteries and decreased injury-induced inflammatory cytokine expression, neutrophil/macrophage infiltration, and neointima formation. Transfused RiPS-ECs overexpressing IL8RA/B and/or CCR2/5 prevented inflammatory responses and neointima formation after vascular injury. Targeted delivery of iPS-ECs with a homing device to inflammatory mediators in injured arteries provides a novel strategy for the treatment of cardiovascular diseases. Stem Cells Translational Medicine 2017;6:1168-1177.

Indexed as

AnimalsCell- and Tissue-Based TherapyEndothelial CellsInduced Pluripotent Stem CellsInflammationMacrophagesMaleNeutrophilsRatsRats, Sprague-DawleyReceptors, CCR2Receptors, CCR5Receptors, Interleukin-8Vascular System InjuriesReceptors, CCR2Receptors, CCR5Receptors, Interleukin-8C-C chemokine receptor 2/5Interleukin 8 receptoriPS-endothelial cellsTargeted cell therapyVascular injury

Identifiers

PMID28233474
PMCPMC5442847
OpenAlexW2589372347

What OpenQuestion holds

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LicenceCC BY
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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.