Evidence map›Paper›PMID 27943413›Full record

ArticleExperimental dermatology2017

Aberrant connective tissue differentiation towards cartilage and bone underlies human keloids in African Americans.

Judilyn Fuentes-Duculan, Kathleen M Bonifacio, Mayte Suárez-Fariñas, Norma Kunjravia, Sandra Garcet, Tristan Cruz, Claire Q F Wang, Hui Xu, Patricia Gilleadeau, Mary Sullivan-Whalen and 2 more

Open access · greenAbstract read
In one paragraph

Article in Experimental dermatology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.0field-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

21 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Article
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  7. Defining a Unique Gene Expression Profile in Mature and Developing Keloids.JID innovations : skin science from molecules to population health · 2023
    Article
  8. [Keloid nomogram prediction model based on weighted gene co-expression network analysis and machine learning].Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi · 2023
    Article
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  17. Genomics of Human Fibrotic Diseases: Disordered Wound Healing Response.International journal of molecular sciences · 2020
    Review
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  19. Article
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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 3 institutions in 2 countries.

Judilyn Fuentes-DuculanLaboratory for Investigative Dermatology, The Rockefeller University, New York, NY, USA.
Kathleen M BonifacioLaboratory for Investigative Dermatology, The Rockefeller University, New York, NY, USA.
Mayte Suárez-FariñasLaboratory for Investigative Dermatology, The Rockefeller University, New York, NY, USA.
Norma KunjraviaLaboratory for Investigative Dermatology, The Rockefeller University, New York, NY, USA.
Sandra GarcetLaboratory for Investigative Dermatology, The Rockefeller University, New York, NY, USA.
Tristan CruzLaboratory for Investigative Dermatology, The Rockefeller University, New York, NY, USA.
Claire Q F WangLaboratory for Investigative Dermatology, The Rockefeller University, New York, NY, USA.
Hui XuDermatology Department, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Patricia GilleadeauLaboratory for Investigative Dermatology, The Rockefeller University, New York, NY, USA.
Mary Sullivan-WhalenLaboratory for Investigative Dermatology, The Rockefeller University, New York, NY, USA.
Michael H TirganLaboratory for Investigative Dermatology, The Rockefeller University, New York, NY, USA.
James G KruegerLaboratory for Investigative Dermatology, The Rockefeller University, New York, NY, USA.
Rockefeller University · USIcahn School of Medicine at Mount Sinai · USBoston Medical Center · US

Funding

TRANSFORMING TRANSLATIONAL SCIENCE AND EDUCATION TO BENEFIT HUMAN HEALTHUL1RR024143 · NCRR · ROCKEFELLER UNIVERSITY · PI COLLER, BARRY · 2006 to 2011
$49.1M
Developing, Demonstrating, and Disseminating Innovative Programs to Achieve Translational SuccessUL1TR001866 · NCATS · ROCKEFELLER UNIVERSITY · PI COLLER, BARRY, KRUEGER, JAMES G · 2016 to 2025
$40.6M
Transforming Translational Science and Education to Benefit Human HealthUL1TR000043 · NCATS · ROCKEFELLER UNIVERSITY · PI COLLER, BARRY · 2012 to 2015
$26.8M
NCATS NIH HHS UL1 TR000043NCATS NIH HHS UL1 TR001866NCRR NIH HHS UL1 RR024143
6 · The paper itself

Abstract

Keloids are benign fibroproliferative tumors more frequently found among African Americans. Until now, keloid etiopathogenesis is not fully understood. To characterize keloids in African Americans, we performed transcriptional profiling of biopsies from large chronic keloids, adjacent non-lesional (NL) skin (n=3) and a newly formed keloid lesion using Affymetrix HGU133 2.0 plus arrays. Quantitative RT-PCR (qRT-PCR) and immunohistochemistry (IHC) staining were performed to confirm increased expression of relevant genes. We identified 1202 upregulated and 961 downregulated differentially expressed genes (DEGs) between keloid and NL skin; 1819 up- and 1867 downregulated DEGs between newly formed keloid and NL skin; and 492 up- and 775 downregulated DEGs between chronic and newly formed keloid (fold change >2, false discovery rate <0.05). Many of the top upregulated DEGs between chronic keloid and NL skin and between newly formed keloid and NL skin are involved in bone/cartilage formation including Fibrillin 2 (FBN2), Collagen type X alpha 1, Asporin (ASPN), Cadherin 11 (CDH11), Bone morphogenic protein 1 (BMP1), Secreted phosphoprotein 1 and Runt-related transcription factor 2 (RUNX2). qRT-PCR confirmed significant (P<.05) upregulation of BMP1, RUNX2, CDH11 and FBN2 in chronic keloid compared to NL skin. IHC staining showed increased protein expression of ASPN, CDH11, BMP1 and RUNX2 on chronic and newly formed keloid compared to NL skin. Our study shows that large keloids in African Americans represent a dysplasia of cutaneous connective tissue towards immature cartilage or bone differentiation. The phenotype is potentially regulated by overexpression of RUNX2. This knowledge may give insights to guide the development of better treatment for the disease in the future.

Indexed as

Cell DifferentiationChondrogenesisBlack or African AmericanConnective TissueGene Expression ProfilingHumansKeloidSkincartilage and bone formationconnective tissue differentiationkeloidtranscriptional profiling

Identifiers

PMID27943413
PMCPMC5466890
OpenAlexW2560712977

What OpenQuestion holds

Textmetadata
LicenceTDM
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.