Evidence map›Paper›PMID 26801304›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2016

Targeted delivery of human iPS-ECs overexpressing IL-8 receptors inhibits neointimal and inflammatory responses to vascular injury in the rat.

Samantha Giordano, Xiangmin Zhao, Daisy Xing, Fadi Hage, Suzanne Oparil, John P Cooke, Jieun Lee, Karina H Nakayama, Ngan F Huang, Yiu-Fai Chen

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
2.0field-weighted citation impact, top 16% 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

8 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
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  5. Article
  6. Review
  7. Myeloid-derived Suppressor Cells Are Necessary for Development of Pulmonary Hypertension.American journal of respiratory cell and molecular biology · 2018
    Article
  8. Article
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 6 institutions in 1 country.

Samantha GiordanoVascular Biology and Hypertension Program, Division of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama;
Xiangmin ZhaoDepartment of Pulmonary, Critical Care, Sleep and Allergy, College of Medicine, University of Illinois at Chicago, Chicago, Illinois;
Daisy XingVascular Biology and Hypertension Program, Division of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama;
Fadi HageVascular Biology and Hypertension Program, Division of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama; Division of Cardiology, Birmingham Veterans Affairs Medical Center, Birmingham, Alabama;
Suzanne OparilVascular Biology and Hypertension Program, Division of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama;
John P CookeHouston Methodist Research Institute, Houston, Texas;
Jieun LeeDivision of Cardiovascular Medicine, Stanford University, Stanford, California;
Karina H NakayamaCardiovascular Institute, Stanford University, Stanford, California; Veterans Affairs Palo Alto Health Care System, Palo Alto, California; and.
Ngan F HuangCardiovascular Institute, Stanford University, Stanford, California; Veterans Affairs Palo Alto Health Care System, Palo Alto, California; and Department of Cardiothoracic Surgery, Stanford University, Stanford, California.
Yiu-Fai ChenVascular Biology and Hypertension Program, Division of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama; yfchen@uab.edu.
University of Alabama at Birmingham · USStanford University · USBirmingham VA Medical Center · USCardiovascular Institute of the South · USHouston Methodist · USUniversity of Illinois Chicago · US

Funding

MECHANISMS OF HYPERTENSION AND CARDIOVASCULAR DISEASEST32HL007457 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Martin E Young · 1985 to 2026
$8.6M
Basic and Translational Research iPSC-based hematologic and vascular therapiesU01HL100397 · NHLBI · STANFORD UNIVERSITY · PI COOKE, JOHN P · 2009 to 2015
$7.4M
T32 Training Program in Mechanisms and Innovation in Vascular DiseaseT32HL098049 · NHLBI · STANFORD UNIVERSITY · PI Nicholas James Leeper, Philip S Tsao · 2010 to 2026
$6.3M
NCE-based strategy for nuclear reprogramming and regenerative medicineRC2HL103400 · NHLBI · STANFORD UNIVERSITY · PI COOKE, JOHN P · 2009 to 2010
$2.7M
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
Matrix-mediated endothelial differentiation of induced pluripotent stem cellsR00HL098688 · NHLBI · PALO ALTO VETERANS INSTIT FOR RESEARCH · PI HUANG, NGAN F. · 2013 to 2016
$742k
NHLBI NIH HHS R00 HL098688NHLBI NIH HHS R00-HL-098688NHLBI NIH HHS R01 HL087980NHLBI NIH HHS R01-HL-087980NHLBI NIH HHS R01 HL116727NHLBI NIH HHS R01-HL-116727NHLBI NIH HHS RC2 HL103400NHLBI NIH HHS RC2-HL-103400NHLBI NIH HHS T32 HL007457NHLBI NIH HHS T32-HL-07457NHLBI NIH HHS T32 HL098049NHLBI NIH HHS U01 HL100397NHLBI NIH HHS U01-HL-100397
6 · The paper itself

Abstract

Interleukin-8 (IL8) is highly expressed by injured arteries in a variety of diseases and is a chemoattractant for neutrophils which express IL8 receptors IL8RA and RB (IL8RA/B) on their membranes. Neutrophils interact with the damaged endothelium and initiate an inflammatory cascade at the site of injury. We have generated a novel translational targeted cell therapy for acute vascular injury using adenoviral vectors to overexpress IL8RA/B and green fluorescent protein (GFP) on the surface of endothelial cells (ECs) derived from human induced pluripotent stem cells (HiPS-IL8RA/B-ECs). We hypothesize that HiPS-IL8RA/B-ECs transfused intravenously into rats with balloon injury of the carotid artery will target to the injured site and compete with neutrophils, thus inhibiting inflammation and neointima formation. Young adult male Sprague-Dawley rats underwent balloon injury of the right carotid artery and received intravenous transfusion of saline vehicle, 1.5 × 10(6) HiPS-ECs, 1.5 × 10(6) HiPS-Null-ECs, or 1.5 × 10(6) HiPS-IL8RA/B-ECs immediately after endoluminal injury. Tissue distribution of HiPS-IL8RA/B-ECs was analyzed by a novel GFP DNA qPCR method. Cytokine and chemokine expression and leukocyte infiltration were measured in injured and uninjured arteries at 24 h postinjury by ELISA and immunohistochemistry, respectively. Neointimal, medial areas, and reendothelialization were measured 14 days postinjury. HiPS-IL8RA/B-ECs homed to injured arteries, inhibited inflammatory mediator expression and inflammatory cell infiltration, accelerated reendothelialization, and attenuated neointima formation after endoluminal injury while control HiPS-ECs and HiPS-Null-ECs did not. HiPS-IL8RA/B-ECs transfused into rats with endoluminal carotid artery injury target to the injured artery and provide a novel strategy to treat vascular injury.

Indexed as

AnimalsCarotid ArteriesCarotid Artery InjuriesCell- and Tissue-Based TherapyEndothelial CellsEnzyme-Linked Immunosorbent AssayGreen Fluorescent ProteinsHumansImmunohistochemistryInduced Pluripotent Stem CellsInflammationMaleNeointimaPolymerase Chain ReactionRatsRats, Sprague-DawleyGreen Fluorescent ProteinsReceptors, Interleukin-8endothelial cellshuman induced pluripotent stem cellsinflammation vascular injuryrestenosistargeted cell therapyvascular injury

Identifiers

PMID26801304
PMCPMC4865064
OpenAlexW2288844450

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.