Evidence map›Paper›PMID 32208424›Full record

ArticlePloS one2020

Assessment of ICAM-1 N-glycoforms in mouse and human models of endothelial dysfunction.

Kellie Regal-McDonald, Maheshika Somarathna, Timmy Lee, Silvio H Litovsky, Jarrod Barnes, J M Peretik, J G Traylor, A Wayne Orr, Rakesh P Patel

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.8field-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

17 citing papers in PubMed, 23 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

9 authors at 2 institutions in 1 country.

Kellie Regal-McDonaldDepartment of Pathology, University of Alabama at Birmingham, Birmingham, Alabama, United States of America.
Maheshika SomarathnaDivision of Nephrology, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, United States of America.
Timmy LeeDivision of Nephrology, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, United States of America.
Silvio H LitovskyDepartment of Pathology, University of Alabama at Birmingham, Birmingham, Alabama, United States of America.
Jarrod BarnesDivision of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, United States of America.
J M PeretikDepartment of Pathology and Translational Pathobiology, Louisiana State University Health Sciences Center, Shreveport, Louisiana, United States of America.
J G TraylorDepartment of Pathology and Translational Pathobiology, Louisiana State University Health Sciences Center, Shreveport, Louisiana, United States of America.
A Wayne OrrDepartment of Pathology and Translational Pathobiology, Louisiana State University Health Sciences Center, Shreveport, Louisiana, United States of America.
Rakesh P PatelDepartment of Pathology, University of Alabama at Birmingham, Birmingham, Alabama, United States of America.ORCID 0000-0002-1526-4303
University of Alabama at Birmingham · USLouisiana State University Health Sciences Center Shreveport · 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
Nitric oxide releasing nanomatrix to enhance dialysis fistula maturationR44DK109789 · NIDDK · ENDOMIMETICS, LLC · PI CHEN, JUN · 2017 to 2022
$3.8M
Nck Adaptor Proteins in Atherogenic Endothelial ActivationR01HL133497 · NHLBI · LOUISIANA STATE UNIV HSC SHREVEPORT · PI ORR, ANTHONY WAYNE · 2016 to 2024
$3.8M
Training Program in Cardiovascular PathophysiologyT32HL007918 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BALLINGER, SCOTT W. · 1999 to 2018
$3.6M
Matrix Signaling in Endothelial Cell DysfunctionR01HL098435 · NHLBI · LOUISIANA STATE UNIV HSC SHREVEPORT · PI ORR, ANTHONY WAYNE · 2010 to 2020
$3.2M
EphA2 signaling in atherosclerotic fibroproliferative remodelingR01HL141155 · NHLBI · LOUISIANA STATE UNIV HSC SHREVEPORT · PI ORR, ANTHONY WAYNE · 2019 to 2022
$1.8M
PRedoctoral Interdisciplinary training in renal physiology and MEdicine (PRIME)T32DK116672 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI POLLOCK, JENNIFER S · 2018 to 2022
$761k
Metabolic drivers and sensors of cell proliferation in pulmonary hypertensionR00HL131866 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BARNES, JARROD W. · 2018 to 2020
$731k
Nitric oxide releasing nanomatrix wrap to enhance dialysis fistula maturationR43DK109789 · NIDDK · ENDOMIMETICS, LLC · PI HWANG, PATRICK, LEE, TIMMY C · 2016 to 2016
$429k
BLRD VA I01 BX003387NHLBI NIH HHS R00 HL131866NHLBI NIH HHS R01 HL098435NHLBI NIH HHS R01 HL133497NHLBI NIH HHS R01 HL141155NHLBI NIH HHS T32 HL007918NIDDK NIH HHS P30 DK079626NIDDK NIH HHS R43 DK109789NIDDK NIH HHS R44 DK109789NIDDK NIH HHS T32 DK116672
6 · The paper itself

Abstract

Endothelial dysfunction is a critical event in vascular inflammation characterized, in part, by elevated surface expression of adhesion molecules such as intercellular adhesion molecule-1 (ICAM-1). ICAM-1 is heavily N-glycosylated, and like other surface proteins, it is largely presumed that fully processed, complex N-glycoforms are dominant. However, our recent studies suggest that hypoglycosylated or high mannose (HM)-ICAM-1 N-glycoforms are also expressed on the cell surface during endothelial dysfunction, and have higher affinity for monocyte adhesion and regulate outside-in endothelial signaling by different mechanisms. Whether different ICAM-1 N-glycoforms are expressed in vivo during disease is unknown. In this study, using the proximity ligation assay, we assessed the relative formation of high mannose, hybrid and complex α-2,6-sialyated N-glycoforms of ICAM-1 in human and mouse models of atherosclerosis, as well as in arteriovenous fistulas (AVF) of patients on hemodialysis. Our data demonstrates that ICAM-1 harboring HM or hybrid epitopes as well as ICAM-1 bearing α-2,6-sialylated epitopes are present in human and mouse atherosclerotic lesions. Further, HM-ICAM-1 positively associated with increased macrophage burden in lesions as assessed by CD68 staining, whereas α-2,6-sialylated ICAM-1 did not. Finally, both HM and α-2,6-sialylated ICAM-1 N-glycoforms were present in hemodialysis patients who had AVF maturation failure compared to successful AVF maturation. Collectively, these data provide evidence that HM- ICAM-1 N-glycoforms are present in vivo, and at levels similar to complex α-2,6-sialylated ICAM-1 underscoring the need to better understand their roles in modulating vascular inflammation.

Indexed as

AdultAgedAnimalsArteriesArteriovenous Shunt, SurgicalAtherosclerosisDisease Models, AnimalEndothelium, VascularEpitopesFemaleGlycosylationHumansHuman Umbilical Vein Endothelial CellsInflammationIntercellular Adhesion Molecule-1MacrophagesEpitopesICAM1 protein, humanIcam1 protein, mouseIntercellular Adhesion Molecule-1MannoseN-Acetylneuraminic AcidProtein Isoforms

Identifiers

PMID32208424
PMCPMC7092995
OpenAlexW3012652893

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.