Evidence map›Paper›PMID 19388012›Full record

ArticleJournal of cellular physiology2009

Retinoid-responsive transcriptional changes in epidermal keratinocytes.

Ding-Dar Lee, Olivera Stojadinovic, Agata Krzyzanowska, Constantinos Vouthounis, Miroslav Blumenberg, Marjana Tomic-Canic

Abstract read
In one paragraph

Article in Journal of cellular physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 2 pooled it
2.8field-weighted citation impact, top 9% 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

61 citing papers in PubMed, 2 syntheses or guidelines pooled it, 119 citations in OpenAlex.

  1. Pooled it
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  8. UTX (KDM6A) promotes differentiation noncatalytically in somatic self-renewing epithelia.Proceedings of the National Academy of Sciences of the United States of America · 2025
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1 more citing papers are in PubMed but not listed here.

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

6 authors at 4 institutions in 2 countries.

Ding-Dar Lee *New York University School of Medicine, Departments of Dermatology, Biochemistry and The Cancer Institute, New York, New York 10016.
Olivera Stojadinovic *Department of Dermatology & Cutaneous Surgery, Wound Healing and Regenerative Medicine Program, University of Miami Miller School of Medicine, Miami, Florida.
Agata KrzyzanowskaHospital for Special Surgery at Weill Medical College of Cornell University, Tissue Repair Lab, Tissue Engineering, Regeneration and Repair Program, New York, New York 10021.
Constantinos VouthounisHospital for Special Surgery at Weill Medical College of Cornell University, Tissue Repair Lab, Tissue Engineering, Regeneration and Repair Program, New York, New York 10021.
Miroslav BlumenbergNew York University School of Medicine, Departments of Dermatology, Biochemistry and The Cancer Institute, New York, New York 10016.
Marjana Tomic-CanicDepartment of Dermatology & Cutaneous Surgery, Wound Healing and Regenerative Medicine Program, University of Miami Miller School of Medicine, Miami, Florida.
Cornell University · USUniversity of Miami · USNational Yang Ming University Hospital · TWNew York University · US

Funding

Epidermal Genes and Their Regulators in Wound HealingR01NR008029 · NINR · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI TOMIC-CANIC, MARJANA · 2003 to 2007
$1.7M
GLUCOCORTICOIDS IN EPIDERMIS: MECHANISMS OF ACTIONR01AR045974 · NIAMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI TOMIC-CANIC, MARJANA · 2000 to 2004
$960k
Development of the Cellular Biomarker for Diabetic Foot UlcersRC1DK086364 · NIDDK · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI BREM, HAROLD, TOMIC-CANIC, MARJANA · 2009 to 2010
$903k
Experimental Model For Pressure Ulcers In Human Skin: The Role of Aging and ECMR21AG030673 · NIA · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI TOMIC-CANIC, MARJANA · 2008 to 2009
$395k
NIAMS NIH HHS AR45974NIAMS NIH HHS R01 AR045974NIA NIH HHS AG030673NIA NIH HHS R21 AG030673NIDDK NIH HHS RC1 DK086364NINR NIH HHS NR08029NINR NIH HHS R01 NR008029
6 · The paper itself

Abstract

Retinoids (RA) have been used as therapeutic agents for numerous skin diseases, from psoriasis to acne and wrinkles. While RA is known to inhibit keratinocyte differentiation, the molecular effects of RA in epidermis have not been comprehensively defined. To identify the transcriptional targets of RA in primary human epidermal keratinocytes, we compared the transcriptional profiles of cells grown in the presence or absence of all-trans retinoic acid for 1, 4, 24, 48, and 72 h, using large DNA microarrays. As expected, RA suppresses the protein markers of cornification; however the genes responsible for biosynthesis of epidermal lipids, long-chain fatty acids, cholesterol, and sphingolipids, are also suppressed. Importantly, the pathways of RA synthesis, esterification and metabolism are activated by RA; therefore, RA regulates its own bioavailability. Unexpectedly, RA regulates many genes associated with the cell cycle and programmed cell death. This led us to reveal novel effects of RA on keratinocyte proliferation and apoptosis. The response to RA is very fast: 315 genes were regulated already after 1 h. More than one-third of RA-regulated genes function in signal transduction and regulation of transcription. Using in silico analysis, we identified a set of over-represented transcription factor binding sites in the RA-regulated genes. Many psoriasis-related genes are regulated by RA, some induced, others suppressed. These results comprehensively document the transcriptional changes caused by RA in keratinocytes, add new insights into the molecular mechanism influenced by RA in the epidermis and demonstrate the hypothesis-generating power of DNA microarray analysis.

Indexed as

Epidermal CellsCell DifferentiationCells, CulturedGene Expression ProfilingGene Expression RegulationHumansKeratinocytesKeratinsKeratolytic AgentsLipid MetabolismMultigene FamilyOligonucleotide Array Sequence AnalysisPromoter Regions, GeneticPsoriasisReceptors, Retinoic AcidTranscription, GeneticKeratinsKeratolytic AgentsReceptors, Retinoic AcidTretinoin

Identifiers

PMID19388012
PMCPMC4386731
OpenAlexW2068062518

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.