Evidence map›Paper›PMID 18818211›Full record

ArticleThe Journal of biological chemistry2008

Specific TRPC6 channel activation, a novel approach to stimulate keratinocyte differentiation.

Margarethe Müller, Kirill Essin, Kerstin Hill, Heike Beschmann, Simone Rubant, Christoph M Schempp, Maik Gollasch, W Henning Boehncke, Christian Harteneck, Walter E Müller and 1 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

43 citing papers in PubMed, 109 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Wound Repair and CaCells · 2024
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  6. Article
  7. Article
  8. Article
  9. Article
  10. Store-operated calcium channels in skin.Frontiers in physiology · 2022
    Review
  11. Article
  12. Review
  13. Article
  14. Anti-Tumor Activity ofAntioxidants (Basel, Switzerland) · 2020
    Review
  15. Review
  16. Article
  17. Article
  18. Molecular mechanisms of mechanotransduction in psoriasis.Annals of translational medicine · 2018
    Review
  19. Skin Barrier and Calcium.Annals of dermatology · 2018
    Review
  20. Article
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

11 authors at 4 institutions in 1 country.

Margarethe MüllerInstitute of Pharmacology, Biocenter Niederursel, Johann Wolfgang Goethe-University, Max-von-Laue-Strasse 9, 60439 Frankfurt, Germany.
Kirill Essin
Kerstin Hill
Heike Beschmann
Simone Rubant
Christoph M Schempp
Maik Gollasch
W Henning Boehncke
Christian Harteneck
Walter E Müller
Kristina Leuner
Goethe University Frankfurt · DECharité - Universitätsmedizin Berlin · DEMax Delbrück Center · DEUniversity Medical Center Freiburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The protective epithelial barrier in our skin undergoes constant regulation, whereby the balance between differentiation and proliferation of keratinocytes plays a major role. Impaired keratinocyte differentiation and proliferation are key elements in the pathophysiology of several important dermatological diseases, including atopic dermatitis and psoriasis. Ca(2+) influx plays an essential role in this process presumably mediated by different transient receptor potential (TRP) channels. However, investigating their individual role was hampered by the lack of specific stimulators or inhibitors. Because we have recently identified hyperforin as a specific TRPC6 activator, we investigated the contribution of TRPC6 to keratinocyte differentiation and proliferation. Like the endogenous differentiation stimulus high extracellular Ca(2+) concentration ([Ca(2+)](o)), hyperforin triggers differentiation in HaCaT cells and in primary cultures of human keratinocytes by inducing Ca(2+) influx via TRPC6 channels and additional inhibition of proliferation. Knocking down TRPC6 channels prevents the induction of Ca(2+)- and hyperforin-induced differentiation. Importantly, TRPC6 activation is sufficient to induce keratinocyte differentiation similar to the physiological stimulus [Ca(2+)](o). Therefore, TRPC6 activation by hyperforin may represent a new innovative therapeutic strategy in skin disorders characterized by altered keratinocyte differentiation.

Indexed as

Bridged Bicyclo CompoundsCalciumCationsCell DifferentiationCell Line, TumorCell ProliferationHumansKeratinocytesModels, BiologicalOrgan Culture TechniquesPhloroglucinolSkinSkin DiseasesTerpenesTime FactorsTransfectionBridged Bicyclo CompoundsCalciumCationshyperforinPhloroglucinolTerpenesTRPC6 Cation ChannelTRPC6 protein, humanTRPC Cation Channels

Identifiers

PMID18818211
PMCPMC2662218
OpenAlexW2017755954

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.