MAP kinase-dependent induction of clock gene expression by α1-adrenergic receptor activation

Masashi Akiyama, Yoichi Minami, Kouji Kuriyama, Shigenobu Shibata

    Research output: Contribution to journalArticle

    20 Citations (Scopus)

    Abstract

    While peripheral oscillators can be reset by humoral factors such as glucocorticoid hormones, indirect neural communications involving sympathetic and parasympathetic neurons from the suprachiasmatic nucleus to various peripheral tissues suggest that autonomic nerve innervations also function in the resetting and synchronization of peripheral tissues. To study the role of sympathetic adrenergic signaling on clock gene expression, we constructed NIH3T3 cells that stably expressed each of three α1-adrenergic receptor subtypes (α1A, α1B and α1D). We found that noradrenaline transiently induced the expression of mPer1, mPer2, and mE4bp4 1-2 h after α1-receptor activation. The extent and time course of clock gene mRNA induction by noradrenaline or the α1-receptor agonist phenylephrine (PE) was similar to that seen by 50% horse serum shock. Clock gene mRNA induction by PE was inhibited by U0126, a MEK inhibitor, suggesting involvement of the mitogen-activated protein kinase signaling pathway. We also found that both mPer1 and mPer2 mRNAs were induced in the mouse liver 60 min after PE injection. These results suggest that although humoral factors are important for entrainment of the peripheral clock, the autonomic nervous system may also be involved in the process.

    Original languageEnglish
    Pages (from-to)109-114
    Number of pages6
    JournalFEBS Letters
    Volume542
    Issue number1-3
    DOIs
    Publication statusPublished - 2003 May 8

    Fingerprint

    Phenylephrine
    Gene expression
    Adrenergic Receptors
    Clocks
    Phosphotransferases
    Chemical activation
    Gene Expression
    Messenger RNA
    Norepinephrine
    Autonomic Pathways
    Suprachiasmatic Nucleus
    Genes
    Autonomic Nervous System
    Mitogen-Activated Protein Kinase Kinases
    Tissue
    Mitogen-Activated Protein Kinases
    Adrenergic Agents
    Glucocorticoids
    Horses
    Shock

    Keywords

    • α-Adrenergic receptor
    • Mitogen-activated protein kinase
    • MPer1
    • MPer2
    • NIH3T3
    • Phenylephrine

    ASJC Scopus subject areas

    • Biochemistry
    • Biophysics
    • Molecular Biology

    Cite this

    MAP kinase-dependent induction of clock gene expression by α1-adrenergic receptor activation. / Akiyama, Masashi; Minami, Yoichi; Kuriyama, Kouji; Shibata, Shigenobu.

    In: FEBS Letters, Vol. 542, No. 1-3, 08.05.2003, p. 109-114.

    Research output: Contribution to journalArticle

    Akiyama, Masashi ; Minami, Yoichi ; Kuriyama, Kouji ; Shibata, Shigenobu. / MAP kinase-dependent induction of clock gene expression by α1-adrenergic receptor activation. In: FEBS Letters. 2003 ; Vol. 542, No. 1-3. pp. 109-114.
    @article{f7e515d5aa1349fabc97d7aee1a94682,
    title = "MAP kinase-dependent induction of clock gene expression by α1-adrenergic receptor activation",
    abstract = "While peripheral oscillators can be reset by humoral factors such as glucocorticoid hormones, indirect neural communications involving sympathetic and parasympathetic neurons from the suprachiasmatic nucleus to various peripheral tissues suggest that autonomic nerve innervations also function in the resetting and synchronization of peripheral tissues. To study the role of sympathetic adrenergic signaling on clock gene expression, we constructed NIH3T3 cells that stably expressed each of three α1-adrenergic receptor subtypes (α1A, α1B and α1D). We found that noradrenaline transiently induced the expression of mPer1, mPer2, and mE4bp4 1-2 h after α1-receptor activation. The extent and time course of clock gene mRNA induction by noradrenaline or the α1-receptor agonist phenylephrine (PE) was similar to that seen by 50{\%} horse serum shock. Clock gene mRNA induction by PE was inhibited by U0126, a MEK inhibitor, suggesting involvement of the mitogen-activated protein kinase signaling pathway. We also found that both mPer1 and mPer2 mRNAs were induced in the mouse liver 60 min after PE injection. These results suggest that although humoral factors are important for entrainment of the peripheral clock, the autonomic nervous system may also be involved in the process.",
    keywords = "α-Adrenergic receptor, Mitogen-activated protein kinase, MPer1, MPer2, NIH3T3, Phenylephrine",
    author = "Masashi Akiyama and Yoichi Minami and Kouji Kuriyama and Shigenobu Shibata",
    year = "2003",
    month = "5",
    day = "8",
    doi = "10.1016/S0014-5793(03)00360-0",
    language = "English",
    volume = "542",
    pages = "109--114",
    journal = "FEBS Letters",
    issn = "0014-5793",
    publisher = "Elsevier",
    number = "1-3",

    }

    TY - JOUR

    T1 - MAP kinase-dependent induction of clock gene expression by α1-adrenergic receptor activation

    AU - Akiyama, Masashi

    AU - Minami, Yoichi

    AU - Kuriyama, Kouji

    AU - Shibata, Shigenobu

    PY - 2003/5/8

    Y1 - 2003/5/8

    N2 - While peripheral oscillators can be reset by humoral factors such as glucocorticoid hormones, indirect neural communications involving sympathetic and parasympathetic neurons from the suprachiasmatic nucleus to various peripheral tissues suggest that autonomic nerve innervations also function in the resetting and synchronization of peripheral tissues. To study the role of sympathetic adrenergic signaling on clock gene expression, we constructed NIH3T3 cells that stably expressed each of three α1-adrenergic receptor subtypes (α1A, α1B and α1D). We found that noradrenaline transiently induced the expression of mPer1, mPer2, and mE4bp4 1-2 h after α1-receptor activation. The extent and time course of clock gene mRNA induction by noradrenaline or the α1-receptor agonist phenylephrine (PE) was similar to that seen by 50% horse serum shock. Clock gene mRNA induction by PE was inhibited by U0126, a MEK inhibitor, suggesting involvement of the mitogen-activated protein kinase signaling pathway. We also found that both mPer1 and mPer2 mRNAs were induced in the mouse liver 60 min after PE injection. These results suggest that although humoral factors are important for entrainment of the peripheral clock, the autonomic nervous system may also be involved in the process.

    AB - While peripheral oscillators can be reset by humoral factors such as glucocorticoid hormones, indirect neural communications involving sympathetic and parasympathetic neurons from the suprachiasmatic nucleus to various peripheral tissues suggest that autonomic nerve innervations also function in the resetting and synchronization of peripheral tissues. To study the role of sympathetic adrenergic signaling on clock gene expression, we constructed NIH3T3 cells that stably expressed each of three α1-adrenergic receptor subtypes (α1A, α1B and α1D). We found that noradrenaline transiently induced the expression of mPer1, mPer2, and mE4bp4 1-2 h after α1-receptor activation. The extent and time course of clock gene mRNA induction by noradrenaline or the α1-receptor agonist phenylephrine (PE) was similar to that seen by 50% horse serum shock. Clock gene mRNA induction by PE was inhibited by U0126, a MEK inhibitor, suggesting involvement of the mitogen-activated protein kinase signaling pathway. We also found that both mPer1 and mPer2 mRNAs were induced in the mouse liver 60 min after PE injection. These results suggest that although humoral factors are important for entrainment of the peripheral clock, the autonomic nervous system may also be involved in the process.

    KW - α-Adrenergic receptor

    KW - Mitogen-activated protein kinase

    KW - MPer1

    KW - MPer2

    KW - NIH3T3

    KW - Phenylephrine

    UR - http://www.scopus.com/inward/record.url?scp=0038743096&partnerID=8YFLogxK

    UR - http://www.scopus.com/inward/citedby.url?scp=0038743096&partnerID=8YFLogxK

    U2 - 10.1016/S0014-5793(03)00360-0

    DO - 10.1016/S0014-5793(03)00360-0

    M3 - Article

    C2 - 12729908

    AN - SCOPUS:0038743096

    VL - 542

    SP - 109

    EP - 114

    JO - FEBS Letters

    JF - FEBS Letters

    SN - 0014-5793

    IS - 1-3

    ER -