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

Masashi Akiyama, Yoichi Minami, Kouji Kuriyama, Shigenobu Shibata*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

22 Citations (Scopus)


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
Issue number1-3
Publication statusPublished - 2003 May 8


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

ASJC Scopus subject areas

  • Biophysics
  • Structural Biology
  • Biochemistry
  • Molecular Biology
  • Genetics
  • Cell Biology


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