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Oxidative stress produced with cell migration increases synthetic phenotype of vascular smooth muscle cells.

Oxidative stress produced with cell migration increases synthetic phenotype of vascular smooth muscle cells. Research Abstract Details 

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  • Oxidative stress produced with cell migration increases synthetic phenotype of vascular smooth muscle cells. Abstract Text:

    hak-joon sungHak-Joon Sung,suzanne g eskinSuzanne G Eskin,yumiko sakuraiYumiko Sakurai,andrew yeeAndrew Yee,noriyuki kataokaNoriyuki Kataoka,larry v mcintireLarry V McIntire,

    Phenotypic modulation of vascular smooth muscle cells (VSMC) and reactive oxygen species (ROS) is important in vascular pathogenesis. Understanding how these factors relate to cell migration can improve design of therapeutic interventions to control vascular disease. We compared the proliferation, protein content and migration of cultured aortic VSMC from wild type (WT) versus transgenic mice (Tgp22phox), in which overexpression of p22phox was targeted to VSMC. Also, we compared H2O2 generation and expression of specific phenotypic markers of non-migrating with migrating WT versus Tgp22phox VSMC in an in vitro wound scratch model. Enhanced H2O2 production in Tgp22phox versus WT VSMC (p < 0.005) significantly correlated with increased protein content, proliferation, and migration. VSMC migrating across the wound edge produced more H2O2 than non-migrating VSMC (p < 0.05). The expression of synthetic phenotypic markers, tropomyosin 4 and myosin heavy chain embryonic (SMemb), was enhanced significantly, while the expression of contractile marker, smooth muscle alpha-actin, was reduced significantly in migrating versus non-migrating cells, and also in Tgp22phox versus WT (p < 0.005) VSMC. These results are consistent with increased production of ROS accelerating the switch from the contractile to the synthetic phenotype, characterized by increases in proliferation, migration, and expression of TM4 and SMemb and decreased alpha-actin.

    Oxidative stress produced with cell migration increases synthetic phenotype of vascular smooth muscle cells. Publishing Authors By Initials

    hj sungHJ Sung,sg eskinSG Eskin,y sakuraiY Sakurai,a yeeA Yee,n kataokaN Kataoka,lv mcintireLV McIntire,

    For similar cardiovascular diseases: vascular diseases research abstracts see: cardiovascular diseases: vascular diseases research

    PUBMED ID PMID:

    MEDLINE DATE:

    Oxidative stress produced with cell migration increases synthetic phenotype of vascular smooth muscle cells. Journal Published:

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

    Journal: Annals of biomedical engineering

    VOLUME: 33

    Page Numbers: 1546-54

    Journal Abbreviation:

    ISSN: 0090-6964

    DAY: 22

    MONTH: Nov

    YEAR: 2005

    Oxidative stress produced with cell migration increases synthetic phenotype of vascular smooth muscle cells. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 361512

    Oxidative stress produced with cell migration increases synthetic phenotype of vascular smooth muscle cells. Keywords Mesh Terms:

    KEYWORDS: Vascular Diseases

    MESH TERMS: therapy

    Chemical & Substance for Abstract: Oxidative stress produced with cell migration increases synthetic phenotype of vascular smooth muscle cells. Information

    Substance Name: NADPH Oxidase

    Registry Number: EC 1.6.3.1

    Grant and Affiliation Information for Oxidative stress produced with cell migration increases synthetic phenotype of vascular smooth muscle cells.

    AFFILIATION: Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, GA 30332, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NHLBI

    GRANT: R21-HL072039

    ACRONYM: HL

    MEDLINETA: Ann Biomed Eng

    REFSOURCE:

    DATABASENAME:

    ACCESSION NUMBER:

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