Evidence map›Paper›PMID 28812215›Full record

ArticleAnnals of biomedical engineering2017

Proteomic Alterations Associated with Biomechanical Dysfunction are Early Processes in the Emilin1 Deficient Mouse Model of Aortic Valve Disease.

P M Angel, D A Narmoneva, M K Sewell-Loftin, C Munjal, L Dupuis, B J Landis, A Jegga, C B Kern, W D Merryman, H S Baldwin and 2 more

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PubMed Full text at PMC Publisher
In one paragraph

Article in Annals of biomedical engineering, 2017. 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
1.1field-weighted citation impact, top 20% 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, 16 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

12 authors at 6 institutions in 2 countries.

P M AngelDepartment of Cell and Molecular Pharmacology & Experimental Therapeutics, Medical University of South Carolina, Charleston, SC, USA.
D A NarmonevaDivision of Biomedical Engineering, University of Cincinnati, Cincinnati, OH, USA.
M K Sewell-LoftinDivision of Biomedical Engineering, Vanderbilt University, Nashville, TN, USA.
C MunjalDivision of Cardiology, Cincinnati Children's Hospital Medical Center, 240 Albert Sabin Way, MLC 7020, Cincinnati, OH, 45229, USA.
L DupuisDepartment of Regenerative Medicine, Medical University of South Carolina, Charleston, SC, USA.
B J LandisDivision of Pediatric Cardiology, Indiana University, Indianapolis, IN, USA.
A JeggaDivision of Biomedical Informatics, Vanderbilt University, Nashville, TN, USA.
C B KernDepartment of Regenerative Medicine, Medical University of South Carolina, Charleston, SC, USA.
W D MerrymanDivision of Biomedical Engineering, Vanderbilt University, Nashville, TN, USA.
H S BaldwinDivision of Pediatric Cardiology, Vanderbilt University, Nashville, TN, USA.
G M BressanDepartment of Molecular Medicine, University of Padua, Padua, Italy.
Robert B HintonDivision of Cardiology, Cincinnati Children's Hospital Medical Center, 240 Albert Sabin Way, MLC 7020, Cincinnati, OH, 45229, USA. bingrbh@icloud.com.
Vanderbilt University · USMedical University of South Carolina · USSabin Vaccine Institute · USIndiana University – Purdue University Indianapolis · USUniversity of Cincinnati · USUniversity of Padua · IT

Funding

Vanderbilt Institute for Clinical and Translational Research (VICTR) -Identifying correlates of functional immunity in SARS-CoV-2 convalescent plasmaUL1TR002243 · NCATS · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Paul A. Harris, Wesley H Self · 2017 to 2026
$130.7M
The Vanderbilt Institute for Clinical and Translational Research (VICTR)UL1TR000445 · NCATS · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BERNARD, GORDON RAPHAEL · 2012 to 2016
$41.4M
LCenter for Clinical and Translational Science and TrainingUL1TR001425 · NCATS · UNIVERSITY OF CINCINNATI · PI MEINZEN-DERR, JAREEN, STRAWN, JEFFREY ROBERT · 2015 to 2024
$37.5M
SOUTH CAROLINA COBRE IN OXIDANTS, REDOX BALANCE AND STRESS SIGNALINGP20GM103542 · NIGMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI WANG, HAIZHEN · 2012 to 2020
$20.2M
Cincinnati Center for Clinical and Translational Sciences and TrainingUL1TR000077 · NCATS · UNIVERSITY OF CINCINNATI · PI HEUBI, JAMES E. · 2012 to 2014
$9.9M
Developmental Determinants of Cardiovascular DiseaseT32HL105334 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BALDWIN, H SCOTT · 2011 to 2021
$4.3M
Tie Tek Modulation of Cardiac DevelopmentR01HL118386 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BALDWIN, H SCOTT · 2013 to 2017
$2.1M
Indiana Pediatric Scientist Award(IPSA)K12HD068371 · NICHD · INDIANA UNIVERSITY INDIANAPOLIS · PI CLAPP, DAVID W · 2013 to 2017
$1.9M
Direct Tumor Glycan Profiling on Tissue MicroarraysR21CA186799 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI DRAKE, RICHARD R. · 2015 to 2016
$496k
Angiogenesis due to Elastic Fiber Fragmentation in Early Aortic Valve Disease-ResR56HL117851 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI HINTON, ROBERT BRUCE · 2014 to 2014
$390k
NCATS NIH HHS UL1 TR000077NCATS NIH HHS UL1 TR000445NCATS NIH HHS UL1 TR001425NCATS NIH HHS UL1 TR002243NCI NIH HHS R21 CA186799NHLBI NIH HHS R01 HL118386NHLBI NIH HHS R56 HL117851NHLBI NIH HHS T32 HL105334NICHD NIH HHS K12 HD068371NIGMS NIH HHS P20 GM103542
6 · The paper itself

Abstract

Aortic valve (AV) disease involves stiffening of the AV cusp with progression characterized by inflammation, fibrosis, and calcification. Here, we examine the relationship between biomechanical valve function and proteomic changes before and after the development of AV pathology in the Emilin1-/- mouse model of latent AV disease. Biomechanical studies were performed to quantify tissue stiffness at the macro (micropipette) and micro (atomic force microscopy (AFM)) levels. Micropipette studies showed that the Emilin1-/- AV annulus and cusp regions demonstrated increased stiffness only after the onset of AV disease. AFM studies showed that the Emilin1-/- cusp stiffens before the onset of AV disease and worsens with the onset of disease. Proteomes from AV cusps were investigated to identify protein functions, pathways, and interaction network alterations that occur with age- and genotype-related valve stiffening. Protein alterations due to Emilin1 deficiency, including changes in pathways and functions, preceded biomechanical aberrations, resulting in marked depletion of extracellular matrix (ECM) proteins interacting with TGFB1, including latent transforming growth factor beta 3 (LTBP3), fibulin 5 (FBLN5), and cartilage intermediate layer protein 1 (CILP1). This study identifies proteomic dysregulation is associated with biomechanical dysfunction as early pathogenic processes in the Emilin1-/- model of AV disease.

Indexed as

AnimalsAortic ValveBicuspid Aortic Valve DiseaseBiomechanical PhenomenaDisease Models, AnimalExtracellular Matrix ProteinsFemaleHeart Defects, CongenitalHeart Valve DiseasesMaleMembrane GlycoproteinsMice, KnockoutProteomicsTransforming Growth Factor beta1elastin microfibril interface located proteinExtracellular Matrix ProteinsMembrane GlycoproteinsTgfb1 protein, mouseTransforming Growth Factor beta1AgingBiomechanicsExtracellular matrixProtein interaction networksProteomicsTGFbeta1Valves

Identifiers

PMID28812215
PMCPMC5665708
OpenAlexW2747694221

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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.