Activation of NMDA receptors promotes dendritic spine development through MMP-mediated ICAM-5 cleavage

Li Tian, Michael Stefanidakis, Lin Ning, Philip Van Lint, Henrietta Nyman-Huttunen, Claude Libert, Shigeyoshi Itohara, Masayoshi Mishina, Heikki Rauvala, Carl G Gahmberg

    Forskningsoutput: TidskriftsbidragArtikelVetenskapligPeer review

    Sammanfattning

    "Matrix metalloproteinase (MMP)-2 and -9 are pivotal in remodeling many tissues. However, their functions and candidate substrates for brain development are poorly characterized. Intercellular adhesion molecule-5 (ICAM-5; Telencephalin) is a neuronal adhesion molecule that regulates dendritic elongation and spine maturation. We find that ICAM-5 is cleaved from hippocampal neurons when the cells are treated with N-methyl-D-aspartic acid (NMDA) or alpha-amino-3-hydroxy5-methylisoxazole-propionic acid (AMPA). The cleavage is blocked by MMP-2 and -9 inhibitors and small interfering RNAs. Newborn MMP-2- and MMP-9-deficient mice brains contain more full-length ICAM-5 than wild-type mice. NMDA receptor activation disrupts the actin cytoskeletal association of ICAM-5, which promotes its cleavage. ICAM-5 is mainly located in dendritic filopodia and immature thin spines. MMP inhibitors block the NMDA-induced cleavage of ICAM-5 more efficiently in dendritic shafts than in thin spines. ICAM-5 deficiency causes retraction of thin spine heads in response to NMDA stimulation. Soluble ICAM-5 promotes elongation of dendritic filopodia from wild-type neurons, but not from ICAM-5-deficient neurons. Thus, MMPs are important for ICAM-5-mediated dendritic spine development."
    Originalspråkengelska
    TidskriftJournal of Cell Biology
    Volym178
    Utgåva4
    Sidor (från-till)687-700
    Antal sidor14
    ISSN0021-9525
    DOI
    StatusPublicerad - 2007
    MoE-publikationstypA1 Tidskriftsartikel-refererad

    Vetenskapsgrenar

    • 311 Basmedicin
    • 118 Biovetenskaper
    • 515 Psykologi

    Citera det här

    Tian, Li ; Stefanidakis, Michael ; Ning, Lin ; Van Lint, Philip ; Nyman-Huttunen, Henrietta ; Libert, Claude ; Itohara, Shigeyoshi ; Mishina, Masayoshi ; Rauvala, Heikki ; Gahmberg, Carl G. / Activation of NMDA receptors promotes dendritic spine development through MMP-mediated ICAM-5 cleavage. I: Journal of Cell Biology. 2007 ; Vol. 178, Nr. 4. s. 687-700.
    @article{637b5d8f1221430980b42da7659a856e,
    title = "Activation of NMDA receptors promotes dendritic spine development through MMP-mediated ICAM-5 cleavage",
    abstract = "{"}Matrix metalloproteinase (MMP)-2 and -9 are pivotal in remodeling many tissues. However, their functions and candidate substrates for brain development are poorly characterized. Intercellular adhesion molecule-5 (ICAM-5; Telencephalin) is a neuronal adhesion molecule that regulates dendritic elongation and spine maturation. We find that ICAM-5 is cleaved from hippocampal neurons when the cells are treated with N-methyl-D-aspartic acid (NMDA) or alpha-amino-3-hydroxy5-methylisoxazole-propionic acid (AMPA). The cleavage is blocked by MMP-2 and -9 inhibitors and small interfering RNAs. Newborn MMP-2- and MMP-9-deficient mice brains contain more full-length ICAM-5 than wild-type mice. NMDA receptor activation disrupts the actin cytoskeletal association of ICAM-5, which promotes its cleavage. ICAM-5 is mainly located in dendritic filopodia and immature thin spines. MMP inhibitors block the NMDA-induced cleavage of ICAM-5 more efficiently in dendritic shafts than in thin spines. ICAM-5 deficiency causes retraction of thin spine heads in response to NMDA stimulation. Soluble ICAM-5 promotes elongation of dendritic filopodia from wild-type neurons, but not from ICAM-5-deficient neurons. Thus, MMPs are important for ICAM-5-mediated dendritic spine development.{"}",
    keywords = "311 Basic medicine, 118 Biological sciences, 515 Psychology",
    author = "Li Tian and Michael Stefanidakis and Lin Ning and {Van Lint}, Philip and Henrietta Nyman-Huttunen and Claude Libert and Shigeyoshi Itohara and Masayoshi Mishina and Heikki Rauvala and Gahmberg, {Carl G}",
    year = "2007",
    doi = "10.1083/jcb.200612097",
    language = "English",
    volume = "178",
    pages = "687--700",
    journal = "Journal of Cell Biology",
    issn = "0021-9525",
    publisher = "Rockefeller university press",
    number = "4",

    }

    Tian, L, Stefanidakis, M, Ning, L, Van Lint, P, Nyman-Huttunen, H, Libert, C, Itohara, S, Mishina, M, Rauvala, H & Gahmberg, CG 2007, 'Activation of NMDA receptors promotes dendritic spine development through MMP-mediated ICAM-5 cleavage', Journal of Cell Biology, vol. 178, nr. 4, s. 687-700. https://doi.org/10.1083/jcb.200612097

    Activation of NMDA receptors promotes dendritic spine development through MMP-mediated ICAM-5 cleavage. / Tian, Li; Stefanidakis, Michael; Ning, Lin; Van Lint, Philip; Nyman-Huttunen, Henrietta; Libert, Claude; Itohara, Shigeyoshi; Mishina, Masayoshi; Rauvala, Heikki; Gahmberg, Carl G.

    I: Journal of Cell Biology, Vol. 178, Nr. 4, 2007, s. 687-700.

    Forskningsoutput: TidskriftsbidragArtikelVetenskapligPeer review

    TY - JOUR

    T1 - Activation of NMDA receptors promotes dendritic spine development through MMP-mediated ICAM-5 cleavage

    AU - Tian, Li

    AU - Stefanidakis, Michael

    AU - Ning, Lin

    AU - Van Lint, Philip

    AU - Nyman-Huttunen, Henrietta

    AU - Libert, Claude

    AU - Itohara, Shigeyoshi

    AU - Mishina, Masayoshi

    AU - Rauvala, Heikki

    AU - Gahmberg, Carl G

    PY - 2007

    Y1 - 2007

    N2 - "Matrix metalloproteinase (MMP)-2 and -9 are pivotal in remodeling many tissues. However, their functions and candidate substrates for brain development are poorly characterized. Intercellular adhesion molecule-5 (ICAM-5; Telencephalin) is a neuronal adhesion molecule that regulates dendritic elongation and spine maturation. We find that ICAM-5 is cleaved from hippocampal neurons when the cells are treated with N-methyl-D-aspartic acid (NMDA) or alpha-amino-3-hydroxy5-methylisoxazole-propionic acid (AMPA). The cleavage is blocked by MMP-2 and -9 inhibitors and small interfering RNAs. Newborn MMP-2- and MMP-9-deficient mice brains contain more full-length ICAM-5 than wild-type mice. NMDA receptor activation disrupts the actin cytoskeletal association of ICAM-5, which promotes its cleavage. ICAM-5 is mainly located in dendritic filopodia and immature thin spines. MMP inhibitors block the NMDA-induced cleavage of ICAM-5 more efficiently in dendritic shafts than in thin spines. ICAM-5 deficiency causes retraction of thin spine heads in response to NMDA stimulation. Soluble ICAM-5 promotes elongation of dendritic filopodia from wild-type neurons, but not from ICAM-5-deficient neurons. Thus, MMPs are important for ICAM-5-mediated dendritic spine development."

    AB - "Matrix metalloproteinase (MMP)-2 and -9 are pivotal in remodeling many tissues. However, their functions and candidate substrates for brain development are poorly characterized. Intercellular adhesion molecule-5 (ICAM-5; Telencephalin) is a neuronal adhesion molecule that regulates dendritic elongation and spine maturation. We find that ICAM-5 is cleaved from hippocampal neurons when the cells are treated with N-methyl-D-aspartic acid (NMDA) or alpha-amino-3-hydroxy5-methylisoxazole-propionic acid (AMPA). The cleavage is blocked by MMP-2 and -9 inhibitors and small interfering RNAs. Newborn MMP-2- and MMP-9-deficient mice brains contain more full-length ICAM-5 than wild-type mice. NMDA receptor activation disrupts the actin cytoskeletal association of ICAM-5, which promotes its cleavage. ICAM-5 is mainly located in dendritic filopodia and immature thin spines. MMP inhibitors block the NMDA-induced cleavage of ICAM-5 more efficiently in dendritic shafts than in thin spines. ICAM-5 deficiency causes retraction of thin spine heads in response to NMDA stimulation. Soluble ICAM-5 promotes elongation of dendritic filopodia from wild-type neurons, but not from ICAM-5-deficient neurons. Thus, MMPs are important for ICAM-5-mediated dendritic spine development."

    KW - 311 Basic medicine

    KW - 118 Biological sciences

    KW - 515 Psychology

    U2 - 10.1083/jcb.200612097

    DO - 10.1083/jcb.200612097

    M3 - Article

    VL - 178

    SP - 687

    EP - 700

    JO - Journal of Cell Biology

    JF - Journal of Cell Biology

    SN - 0021-9525

    IS - 4

    ER -