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Expression and function of COOH-terminal myosin heavy chain isoforms in mouse smooth muscle.

Expression and function of COOH-terminal myosin heavy chain isoforms in mouse smooth muscle. Research Abstract Details 

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  • Expression and function of COOH-terminal myosin heavy chain isoforms in mouse smooth muscle. Abstract Text:

    anne f martinAnne F Martin,sunita bhattiSunita Bhatti,gail j pyne-geithmanGail J Pyne-Geithman,mariam farjahMariam Farjah,vlasios manavesVlasios Manaves,lori walkerLori Walker,roberta franksRoberta Franks,arthur r strauchArthur R Strauch,richard j paulRichard J Paul,

    Isoforms of the smooth muscle myosin motor, SM1 and SM2, differ in length at the carboxy terminal tail region. Their proportion changes with development, hormonal status and disease, but their function is unknown. We developed mice carrying the myosin heavy chain (MyHC) transgenes SM1, cMyc-tagged SM1, SM2, and V5-tagged SM2, and all transgenes corresponded to the SMa NH(2)-terminal isoform. Transgene expression was targeted to smooth muscle by the smooth muscle alpha-actin promoter. Immunoblot analysis showed substantial expression of the cMyc-tagged SM1 and V5-tagged SM2 MyHC protein in aorta and bladder and transgene mRNA was expressed in mice carrying unlabeled SM1 or SM2 transgenes. Despite significant protein expression of tagged MyHCs we found only small changes in the SM1:SM2 protein ratio. Significant changes in functional phenotype were observed in mice carrying unlabeled SM1 or SM2 transgenes. Force in aorta and bladder was increased (72 +/- 14%, 92 +/- 11%) in SM1 and decreased to 57 +/- 1% and 80 +/- 3% in SM2 transgenic mice. SM1 transgenic bladders had faster (1.8 +/- 0.3 s) and SM2 slower (7.1 +/- 0.5 s) rates of force redevelopment following a rapid step shortening. We hypothesize that small changes in the SM1:SM2 ratio could be amplified if they are associated with changes in thick filament assembly and underlie the altered contractility. These data provide evidence indicating an in vivo function for the COOH-terminal isoforms of smooth muscle myosin and suggest that the SM1:SM2 ratio is tightly regulated in smooth muscle tissues.

    Expression and function of COOH-terminal myosin heavy chain isoforms in mouse smooth muscle. Publishing Authors By Initials

    af martinAF Martin,s bhattiS Bhatti,gj pyne-geithmanGJ Pyne-Geithman,m farjahM Farjah,v manavesV Manaves,l walkerL Walker,r franksR Franks,ar strauchAR Strauch,rj paulRJ Paul,

    For similar urogenital system: urinary tract: urinary bladder research abstracts see: urogenital system: urinary tract: urinary bladder research

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    Expression and function of COOH-terminal myosin heavy chain isoforms in mouse smooth muscle. Journal Published:

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

    Journal: American journal of physiology. Cell physiology

    VOLUME: 293

    Page Numbers: C238-45

    Journal Abbreviation: Am. J. Physiol., Cell Physiol.

    ISSN: 0363-6143

    DAY: 28

    MONTH: 03

    YEAR: 2007

    Expression and function of COOH-terminal myosin heavy chain isoforms in mouse smooth muscle. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 100901225

    Expression and function of COOH-terminal myosin heavy chain isoforms in mouse smooth muscle. Keywords Mesh Terms:

    KEYWORDS: Urinary Bladder

    MESH TERMS: metabolism

    Chemical & Substance for Abstract: Expression and function of COOH-terminal myosin heavy chain isoforms in mouse smooth muscle. Information

    Substance Name: Smooth Muscle Myosins

    Registry Number: EC 3.6.1.-

    Grant and Affiliation Information for Expression and function of COOH-terminal myosin heavy chain isoforms in mouse smooth muscle.

    AFFILIATION: Dept. of Physiology and Biophysics, University of Illinois at Chicago, 835 S. Wolcott Ave., Chicago, IL 60612, USA. afmartin@uic.edu

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NHLBI

    GRANT: HL-64942

    ACRONYM: HL

    MEDLINETA: Am J Physiol Cell Physiol

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