Evidence map›Paper›PMID 15263021›Full record

ArticleThe Journal of cell biology2004

Novel signaling pathways mediating reciprocal control of keratinocyte migration and wound epithelialization through M3 and M4 muscarinic receptors.

Alex I Chernyavsky, Juan Arredondo, Jürgen Wess, Evert Karlsson, Sergei A Grando

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.9field-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

34 citing papers in PubMed, 83 citations in OpenAlex.

  1. Article
  2. The Role of Muscarinic Acetylcholine Receptor MInternational journal of molecular sciences · 2024
    Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Extrasynaptic acetylcholine signaling through a muscarinic receptor regulates cell migration.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
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  17. Article
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  20. 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

5 authors at 3 institutions in 2 countries.

Alex I ChernyavskyDeppartment of Dermatology, University of California, Davis, Sacramento, CA 95817, USA.
Juan Arredondo
Jürgen Wess
Evert Karlsson
Sergei A Grando
University of California, Davis · USKarolinska Institutet · SENational Institute of Diabetes and Digestive and Kidney Diseases · US

Funding

Epithelial Acetylcholine Oral Biology and PathologyR01DE014173 · NIDCR · UNIVERSITY OF CALIFORNIA-IRVINE · PI GRANDO, SERGEI A · 2002 to 2012
$3.1M
Regulation of Keratinocyte Migration by AcetylcholineR01GM062136 · NIGMS · UNIVERSITY OF CALIFORNIA-IRVINE · PI GRANDO, SERGEI A · 2002 to 2010
$1.9M
STUDIES ON NEUROTRANSMITTER RECEPTOR GENESZ01DK032003 · NIDDK · DIABETES, DIGESTIVE, KIDNEY DISEASES · PI WESS, JURGEN · 1993 to 2006
–
NIDCR NIH HHS DE14173NIDCR NIH HHS R01 DE014173NIGMS NIH HHS GM62136NIGMS NIH HHS R01 GM062136
6 · The paper itself

Abstract

To test the hypothesis that keratinocyte (KC) migration is modulated by distinct muscarinic acetylcholine (ACh) receptor subtypes, we inactivated signaling through specific receptors in in vitro and in vivo models of reepithelialization by subtype-selective antagonists, small interfering RNA, and gene knockout in mice. KC migration and wound reepithelialization were facilitated by M4 and inhibited by M3. Additional studies showed that M4 increases expression of "migratory" integrins alpha5beta1, alphaVbeta5, and alphaVbeta6, whereas M3 up-regulates "sedentary" integrins alpha2beta1 and alpha3beta1. Inhibition of migration by M3 was mediated through Ca2+-dependent guanylyl cyclase-cyclic GMP-protein kinase G signaling pathway. The M4 effects resulted from inhibition of the inhibitory pathway involving the adenylyl cyclase-cyclic AMP-protein kinase A pathway. Both signaling pathways intersected at Rho, indicating that Rho kinase provides a common effector for M3 and M4 regulation of cell migration. These findings offer novel insights into the mechanisms of ACh-mediated modulation of KC migration and wound reepithelialization, and may aid the development of novel methods to promote wound healing.

Indexed as

Signal TransductionWound HealingAnimalsCell MovementEpithelial CellsHumansIntegrinsKeratinocytesMiceMice, KnockoutReceptor, Muscarinic M3Receptor, Muscarinic M4rho GTP-Binding ProteinsUp-RegulationIntegrinsReceptor, Muscarinic M3Receptor, Muscarinic M4rho GTP-Binding Proteins

Identifiers

PMID15263021
PMCPMC2172302
OpenAlexW2111732097

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.