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Intercellular adhesion molecule-1 deficiency attenuates the development of skin fibrosis in tight-skin mice.

Intercellular adhesion molecule-1 deficiency attenuates the development of skin fibrosis in tight-skin mice. Research Abstract Details 

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  • Intercellular adhesion molecule-1 deficiency attenuates the development of skin fibrosis in tight-skin mice. Abstract Text:

    yukiyo matsushitaYukiyo Matsushita,minoru hasegawaMinoru Hasegawa,takashi matsushitaTakashi Matsushita,manabu fujimotoManabu Fujimoto,mayuka horikawaMayuka Horikawa,tomoyuki fujitaTomoyuki Fujita,ayako kawasujiAyako Kawasuji,fumihide ogawaFumihide Ogawa,douglas a steeberDouglas A Steeber,thomas f tedderThomas F Tedder,kazuhiko takeharaKazuhiko Takehara,shinichi satoShinichi Sato,

    The tight-skin (TSK/+) mouse, a genetic model for systemic sclerosis, develops cutaneous fibrosis. Although a fibrillin 1 gene mutation and immunological abnormalities have been demonstrated, the roles of adhesion molecules have not been investigated. To directly assess roles of adhesion molecules in skin fibrosis, TSK/+ mice lacking L-selectin and/or ICAM-1 were generated. The deficiency of ICAM-1, but not L-selectin, significantly suppressed ( approximately 48%) the development of skin sclerosis in TSK/+ mice. Similarly, ICAM-1 antisense oligonucleotides inhibited skin fibrosis in TSK/+ mice. Although T cell infiltration was modest into the skin of TSK/+ mice, ICAM-1 deficiency down-regulated this migration, which is consistent with the established roles of endothelial ICAM-1 in leukocyte infiltration. In addition, altered phenotype or function of skin fibroblasts was remarkable and dependent on ICAM-1 expression in TSK/+ mice. ICAM-1 expression was augmented on TSK/+ dermal fibroblasts stimulated with IL-4. Although growth or collagen synthesis of TSK/+ fibroblasts cultured with IL-4 was up-regulated, it was suppressed by the loss or blocking of ICAM-1. Collagen expression was dependent on the strain of fibroblasts, but not on the strain of cocultured T cells. Thus, our findings indicate that ICAM-1 expression contributes to the development of skin fibrosis in TSK/+ mice, especially via ICAM-1 expressed on skin fibroblasts.

    Intercellular adhesion molecule-1 deficiency attenuates the development of skin fibrosis in tight-skin mice. Publishing Authors By Initials

    y matsushitaY Matsushita,m hasegawaM Hasegawa,t matsushitaT Matsushita,m fujimotoM Fujimoto,m horikawaM Horikawa,t fujitaT Fujita,a kawasujiA Kawasuji,f ogawaF Ogawa,da steeberDA Steeber,tf tedderTF Tedder,k takeharaK Takehara,s satoS Sato,

    For similar genetic processes: gene expression regulation: up-regulation research abstracts see: genetic processes: gene expression regulation: up-regulation research

    PUBMED ID PMID:

    MEDLINE DATE:

    Intercellular adhesion molecule-1 deficiency attenuates the development of skin fibrosis in tight-skin mice. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    VOLUME: 179

    Page Numbers: 698-707

    Journal Abbreviation: J. Immunol.

    ISSN: 0022-1767

    DAY: 1

    MONTH: Jul

    YEAR: 2007

    Intercellular adhesion molecule-1 deficiency attenuates the development of skin fibrosis in tight-skin mice. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 2985117

    Intercellular adhesion molecule-1 deficiency attenuates the development of skin fibrosis in tight-skin mice. Keywords Mesh Terms:

    KEYWORDS: Up-Regulation

    MESH TERMS: immunology

    Chemical & Substance for Abstract: Intercellular adhesion molecule-1 deficiency attenuates the development of skin fibrosis in tight-skin mice. Information

    Substance Name: Collagen

    Registry Number: 9007-34-5

    Grant and Affiliation Information for Intercellular adhesion molecule-1 deficiency attenuates the development of skin fibrosis in tight-skin mice.

    AFFILIATION: Department of Dermatology, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NCI

    GRANT: CA96547

    ACRONYM: CA

    MEDLINETA: J Immunol

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