Evidence map›Paper›PMID 33991687›Full record

ArticleMolecular & cellular proteomics : MCP2021

Reverse Phase Protein Array Reveals Correlation of Retinoic Acid Metabolism With Cardiomyopathy in Friedreich's Ataxia.

Jill S Napierala, Kimal Rajapakshe, Amanda Clark, Yu-Yun Chen, Shixia Huang, Clementina Mesaros, Peining Xu, Ian A Blair, Lauren A Hauser, Jennifer Farmer and 4 more

Open access · goldAbstract read
In one paragraph

Article in Molecular & cellular proteomics : MCP, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.8field-weighted citation impact, top 33% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Skeletal Muscle Involvement in Friedreich Ataxia.International journal of molecular sciences · 2024
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
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

14 authors at 5 institutions in 1 country.

Jill S NapieralaDepartment of Biochemistry and Molecular Genetics, University of Alabama at Birmingham, Birmingham, Alabama, USA. Electronic address: jsbutler@uab.edu.
Kimal RajapaksheDepartment of Molecular and Cellular Biology, Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, Texas, USA.
Amanda ClarkDepartment of Biochemistry and Molecular Genetics, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Yu-Yun ChenDepartment of Biochemistry and Molecular Genetics, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Shixia HuangDepartment of Molecular and Cellular Biology, Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, Texas, USA.
Clementina MesarosDepartment of Systems Pharmacology and Translational Therapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Peining XuDepartment of Systems Pharmacology and Translational Therapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Ian A BlairDepartment of Systems Pharmacology and Translational Therapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Lauren A HauserDivision of Neurology, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA.
Jennifer FarmerFriedreich's Ataxia Research Alliance, Downingtown, Pennsylvania, USA.
David R LynchDivision of Neurology, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA.
Dean P EdwardsDepartment of Molecular and Cellular Biology, Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, Texas, USA.
Cristian CoarfaDepartment of Molecular and Cellular Biology, Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, Texas, USA.
Marek NapieralaDepartment of Biochemistry and Molecular Genetics, University of Alabama at Birmingham, Birmingham, Alabama, USA. Electronic address: mnapiera@uab.edu.
Baylor College of Medicine · USUniversity of Alabama at Birmingham · USTranslational Therapeutics (United States) · USChildren's Hospital of Philadelphia · USFriedreich's Ataxia Research Alliance · US

Funding

Tumor BiologyP30CA125123 · NCI · BAYLOR COLLEGE OF MEDICINE · PI Suzanne AW Fuqua · 2007 to 2026
$73.9M
GAA REPEATS INDUCED EPIGENETIC SILENCING IN FRIEDREICH'S ATAXIAR01NS081366 · NINDS · UT SOUTHWESTERN MEDICAL CENTER · PI NAPIERALA, MAREK · 2012 to 2021
$3.7M
Defining the impact of Frataxin point mutations on Friedreich's ataxia pathogenesisR01NS121038 · NINDS · UT SOUTHWESTERN MEDICAL CENTER · PI NAPIERALA, MAREK · 2021 to 2025
$2.0M
NCI NIH HHS P30 CA125123NINDS NIH HHS R01 NS081366NINDS NIH HHS R01 NS121038
6 · The paper itself

Abstract

Identifying biomarkers is important for assessment of disease progression, prediction of symptom development, and determination of treatment effectiveness. While unbiased analyses of differential gene expression using next-generation sequencing methods are now routinely conducted, proteomics studies are more challenging because of traditional methods predominantly being low throughput and offering a limited dynamic range for simultaneous detection of hundreds of proteins that drastically differ in their intracellular abundance. We utilized a sensitive and high-throughput proteomic technique, reverse phase protein array (RPPA), to attain protein expression profiles of primary fibroblasts obtained from patients with Friedreich's ataxia (FRDA) and unaffected controls (CTRLs). The RPPA was designed to detect 217 proteins or phosphorylated proteins by individual antibody, and the specificity of each antibody was validated prior to the experiment. Among 62 fibroblast samples (44 FRDA and 18 CTRLs) analyzed, 30 proteins/phosphoproteins were significantly changed in FRDA fibroblasts compared with CTRL cells (p < 0.05), mostly representing signaling molecules and metabolic enzymes. As expected, frataxin was significantly downregulated in FRDA samples, thus serving as an internal CTRL for assay integrity. Extensive bioinformatics analyses were conducted to correlate differentially expressed proteins with critical disease parameters (e.g., selected symptoms, age of onset, guanine-adenine-adenine sizes, frataxin levels, and Functional Assessment Rating Scale scores). Members of the integrin family of proteins specifically associated with hearing loss in FRDA. Also, RPPA data, combined with results of transcriptome profiling, uncovered defects in the retinoic acid metabolism pathway in FRDA samples. Moreover, expression of aldehyde dehydrogenase family 1 member A3 differed significantly between cardiomyopathy-positive and cardiomyopathy-negative FRDA cohorts, demonstrating that metabolites such as retinol, retinal, or retinoic acid could become potential predictive biomarkers of cardiac presentation in FRDA.

Indexed as

AdolescentAdultAgedAldehyde OxidoreductasesBiomarkersCardiomyopathiesCells, CulturedFemaleFibroblastsFrataxinFriedreich AtaxiaHumansIron-Binding ProteinsMaleMiddle AgedProtein Array Analysisaldehyde dehydrogenase (NAD(P)+)Aldehyde OxidoreductasesBiomarkersFrataxinIron-Binding ProteinsRetinoidsbiomarkerfrataxinFriedreich's ataxiaintegrinsretinoid metabolismreverse phase protein array

Identifiers

PMID33991687
PMCPMC8214145
OpenAlexW3163184542

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.