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Mice lacking smooth muscle calponin display increased bone formation that is associated with enhancement of bone morphogenetic protein responses.

Mice lacking smooth muscle calponin display increased bone formation that is associated with enhancement of bone morphogenetic protein responses. Research Abstract Details 

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  • Mice lacking smooth muscle calponin display increased bone formation that is associated with enhancement of bone morphogenetic protein responses. Abstract Text:

    h yoshikawaH Yoshikawa,s i taniguchiS I Taniguchi,h yamamuraH Yamamura,s moriS Mori,m sugimotoM Sugimoto,k miyadoK Miyado,k nakamuraK Nakamura,k nakaoK Nakao,m katsukiM Katsuki,n shibataN Shibata,k takahashiK Takahashi,

    BACKGROUND: Calponin is a calmodulin-and actin-binding protein expressed in smooth muscle. It promotes actin polymerization and inhibits actin-activated myosin ATPase activity. Despite the molecular and functional characterization of calponin in vitro, the physiological role of calponin in vivo has not been clarified. RESULTS: We investigated the in vivo function of smooth muscle calponin (also called basic calponin or calponin h1) by generating mice carrying a targeted mutation in both alleles of the calponin gene. Mice lacking basic calponin expression displayed enhanced ectopic bone formation in vivo, induced by recombinant human bone morphogenetic protein-2 (rhBMP-2), and an augmentation of the degree of osteoblastic differentiation of embryonic mesenchymal cells when they were stimulated by rhBMP-2. Basic calponin messenger RNA was shown to be expressed in developing and healing bone tissues, and in undifferentiated MC3T3-E1 osteoblasts. An examination of the skeletons of mutated mice showed an early onset of cartilage formation and ossification, and increased postnatal bone formation characterized by an increase in the number of activated periosteal osteoblasts. Bone fracture healing was accelerated in mutated mice. CONCLUSION: This is the first demonstration of animals with enhanced BMP responsiveness in host cells, suggesting that endogenous basic calponin may play a negative role in an osteogenic programme.

    Mice lacking smooth muscle calponin display increased bone formation that is associated with enhancement of bone morphogenetic protein responses. Publishing Authors By Initials

    h yoshikawaH Yoshikawa,si taniguchiSI Taniguchi,h yamamuraH Yamamura,s moriS Mori,m sugimotoM Sugimoto,k miyadoK Miyado,k nakamuraK Nakamura,k nakaoK Nakao,m katsukiM Katsuki,n shibataN Shibata,k takahashiK Takahashi,

    For similar peptides: intercellular signaling peptides and proteins: cytokines: transforming growth factor beta research abstracts see: peptides: intercellular signaling peptides and proteins: cytokines: transforming growth factor beta research

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    Mice lacking smooth muscle calponin display increased bone formation that is associated with enhancement of bone morphogenetic protein responses. Journal Published:

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

    Journal: Genes to cells : devoted to molecular & cellular m

    VOLUME: 3

    Page Numbers: 685-95

    Journal Abbreviation: Genes Cells

    ISSN: 1356-9597

    DAY: 19

    MONTH: Oct

    YEAR: 1998

    Mice lacking smooth muscle calponin display increased bone formation that is associated with enhancement of bone morphogenetic protein responses. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 9607379

    Mice lacking smooth muscle calponin display increased bone formation that is associated with enhancement of bone morphogenetic protein responses. Keywords Mesh Terms:

    KEYWORDS: Transforming Growth Factor beta

    MESH TERMS: metabolism

    Chemical & Substance for Abstract: Mice lacking smooth muscle calponin display increased bone formation that is associated with enhancement of bone morphogenetic protein responses. Information

    Substance Name: calponin

    Registry Number: 0

    Grant and Affiliation Information for Mice lacking smooth muscle calponin display increased bone formation that is associated with enhancement of bone morphogenetic protein responses.

    AFFILIATION: Department of Orthopaedic Surgery, Osaka Medical Center for Cancer and Cardiovascular Diseases, Osaka, Osaka 537-8511, Japan.

    Country: ENGLAND

    ENGLAND Research PublicationENGLAND Research Publication

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    MEDLINETA: Genes Cells

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