Evidence map›Paper›PMID 19307725›Full record

ArticleThe Journal of clinical investigation2009

Loss of serum response factor in keratinocytes results in hyperproliferative skin disease in mice.

Heidi Koegel, Lukas von Tobel, Matthias Schäfer, Siegfried Alberti, Elisabeth Kremmer, Cornelia Mauch, Daniel Hohl, Xiao-Jing Wang, Hans-Dietmar Beer, Wilhelm Bloch and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.0field-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

28 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
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  11. Endothelial depletion of murine SRF/MRTF provokes intracerebral hemorrhagic stroke.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  12. Article
  13. Activation of MRTF-A-dependent gene expression with a small molecule promotes myofibroblast differentiation and wound healing.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  14. Article
  15. Article
  16. Serum response factor is required for cortical axon growth but is dispensable for neurogenesis and neocortical lamination.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011
    Article
  17. Review
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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 5 institutions in 2 countries.

Heidi KoegelInstitute of Cell Biology, Department of Biology, ETH Zürich, Zürich, Switzerland.
Lukas von Tobel
Matthias Schäfer
Siegfried Alberti
Elisabeth Kremmer
Cornelia Mauch
Daniel Hohl
Xiao-Jing Wang
Hans-Dietmar Beer
Wilhelm Bloch
Alfred Nordheim
Sabine Werner
ETH Zurich · CHUniversity of Tübingen · DEGerman Sport University Cologne · DEHelmholtz Zentrum München · DEUniversity of Cologne · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The transcription factor serum response factor (SRF) plays a crucial role in the development of several organs. However, its role in the skin has not been explored. Here, we show that keratinocytes in normal human and mouse skin expressed high levels of SRF but that SRF expression was strongly downregulated in the hyperproliferative epidermis of wounded and psoriatic skin. Keratinocyte-specific deletion within the mouse SRF locus during embryonic development caused edema and skin blistering, and all animals died in utero. Postnatal loss of mouse SRF in keratinocytes resulted in the development of psoriasis-like skin lesions. These lesions were characterized by inflammation, hyperproliferation, and abnormal differentiation of keratinocytes as well as by disruption of the actin cytoskeleton. Ultrastructural analysis revealed markedly reduced cell-cell and cell-matrix contacts and loss of cell compaction in all epidermal layers. siRNA-mediated knockdown of SRF in primary human keratinocytes revealed that the cytoskeletal abnormalities and adhesion defects were a direct consequence of the loss of SRF. In contrast, the hyperproliferation observed in vivo was an indirect effect that was most likely a consequence of the inflammation. These results reveal that loss of SRF disrupts epidermal homeostasis and strongly suggest its involvement in the pathogenesis of hyperproliferative skin diseases, including psoriasis.

Indexed as

ActinsAnimalsBase SequenceCell AdhesionCell DifferentiationCell MovementCell ProliferationCells, CulturedDesmosomesDNA PrimersDown-RegulationFemaleHumansKeratinocytesMiceMice, Mutant StrainsActinsDNA PrimersRNA, Small InterferingSerum Response FactorSRF protein, human

Identifiers

PMID19307725
PMCPMC2662566
OpenAlexW2049581032

What OpenQuestion holds

Textmetadata
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.