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Kit signaling is essential for development and maintenance of interstitial cells of Cajal and electrical rhythmicity in the embryonic gastrointestinal tract.

Kit signaling is essential for development and maintenance of interstitial cells of Cajal and electrical rhythmicity in the embryonic gastrointestinal tract. Research Abstract Details 

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  • Kit signaling is essential for development and maintenance of interstitial cells of Cajal and electrical rhythmicity in the embryonic gastrointestinal tract. Abstract Text:

    elizabeth a h beckettElizabeth A H Beckett,seungil roSeungil Ro,yulia bayguinovYulia Bayguinov,kenton m sandersKenton M Sanders,sean m wardSean M Ward,

    Interstitial cells of Cajal (ICC) are specialized cells in smooth muscle organs that generate and propagate pacemaker activity, receive inputs from motor neurons, and serve as mechanosensors. In the gastrointestinal tract, development and maintenance of the ICC phenotype have been linked to intracellular signaling via Kit, but its role in development of ICC during embryogenesis is controversial. Here we have studied the development of functional ICC-MY during the late gestational period in mice. Blocking Kit with a neutralizing antibody before and after development of spontaneous electrical activity (E17 to P0) caused loss of ICC-MY networks and pacemaker activity. ICC-MY and pacemaker activity developed normally in W/+ and W(V)/+ heterozygotes, but failed to develop between E17 to P0 in W/W(V) embryos with compromised Kit function. Muscles treated with Kit neutralizing antibody or the tyrosine kinase inhibitor, imatinib mesylate (STI571), from E17-P0 for 3 days caused loss of functionally developed ICC-MY networks, but ICC-MY and pacemaker activity recovered within 9 days after discontinuing treatment with neutralizing antibody or imatinib mesylate. These data suggest that Kit signaling is an important factor in lineage decision and in the development of functional ICC in late gestation. ICC-MY demonstrate significant plasticity in gastrointestinal tissues. Manipulation of the ICC phenotype might provide useful therapies in gastrointestinal disease where the Kit-positive cell population is either lost or amplified.

    Kit signaling is essential for development and maintenance of interstitial cells of Cajal and electrical rhythmicity in the embryonic gastrointestinal tract. Publishing Authors By Initials

    ea beckettEA Beckett,s roS Ro,y bayguinovY Bayguinov,km sandersKM Sanders,sm wardSM Ward,

    For similar synaptic transmission research abstracts see: synaptic transmission research

    PUBMED ID PMID:

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    Kit signaling is essential for development and maintenance of interstitial cells of Cajal and electrical rhythmicity in the embryonic gastrointestinal tract. Journal Published:

    PUBLICATION TYPE: Research Support, N.I.H., Extr

    Journal: Developmental dynamics : an official publication o

    VOLUME: 236

    Page Numbers: 60-72

    Journal Abbreviation: Dev. Dyn.

    ISSN: 1058-8388

    DAY: 3

    MONTH: Jan

    YEAR: 2007

    Kit signaling is essential for development and maintenance of interstitial cells of Cajal and electrical rhythmicity in the embryonic gastrointestinal tract. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 9201927

    Kit signaling is essential for development and maintenance of interstitial cells of Cajal and electrical rhythmicity in the embryonic gastrointestinal tract. Keywords Mesh Terms:

    KEYWORDS: Synaptic Transmission

    MESH TERMS: metabolism

    Chemical & Substance for Abstract: Kit signaling is essential for development and maintenance of interstitial cells of Cajal and electrical rhythmicity in the embryonic gastrointestinal tract. Information

    Substance Name: Proto-Oncogene Proteins c-kit

    Registry Number: EC 2.7.1.112

    Grant and Affiliation Information for Kit signaling is essential for development and maintenance of interstitial cells of Cajal and electrical rhythmicity in the embryonic gastrointestinal tract.

    AFFILIATION: Department of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, Nevada 89557, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NIDDK

    GRANT: DK 41315

    ACRONYM: DK

    MEDLINETA: Dev Dyn

    REFSOURCE:

    DATABASENAME:

    ACCESSION NUMBER:

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