title: The epinephrine increases tyrosine hydroxylase expression through upregulating thioredoxin-1 in PC12 cells.
abstract: Epinephrine is a stress hormone which is sharply increased in response to acute stress and is continuously elevated during persistent stress. Thioredoxin-1 (Trx-1) is a redox regulating protein and is induced under various stresses. Our previous study has shown that epinephrine induces the expression of Trx-1. Tyrosine hydroxylase (TH) is the major rate-limiting enzyme in catecholamine biosynthesis in response to stress. However, how TH is regulated by epinephrine is still unknown. In the present study, we found that epinephrine increased the expression of TH in a dose- and time-dependent manner in PC12 cells, which was inhibited by propranolol (β-adrenergic receptor inhibitor), but not by phenoxybenzamine (α-adrenergic receptor inhibitor). The increase of TH was also inhibited by SQ22536 (adenylyl cyclase inhibitor), H-89(PKA inhibitor) and LY294002 (phosphatidylinositol 3 kinase inhibitor). More importantly, overexpression of Trx-1 significantly enhanced the expression of TH, while Trx-1 siRNA suppressed TH expression induced by epinephrine. These results suggest that Trx-1 is involved in TH expression induced by epinephrine in PC12 cells.
authors.affiliation: Laboratory of Molecular Neurobiology, Medical Faculty, Kunming University of Science and Technology, Kunming 650500, China.
authors.forename: Jin-Jing
authors.initials: JJ
authors.lastname: Jia
authors.affiliation: Laboratory of Molecular Neurobiology, Medical Faculty, Kunming University of Science and Technology, Kunming 650500, China.
authors.forename: Xian-Si
authors.initials: XS
authors.lastname: Zeng
authors.affiliation: Laboratory of Molecular Neurobiology, Medical Faculty, Kunming University of Science and Technology, Kunming 650500, China.
authors.forename: Li-Hua
authors.initials: LH
authors.lastname: Yang
authors.affiliation: Laboratory of Molecular Neurobiology, Medical Faculty, Kunming University of Science and Technology, Kunming 650500, China. Electronic address: jiebai662001@126.com.
authors.forename: Jie
authors.initials: J
authors.lastname: Bai
mesh_terms: D000818:Animals; D000242:Cyclic AMP / Q000378:metabolism; D017868:Cyclic AMP-Dependent Protein Kinases / Q000378:metabolism; D004837:Epinephrine / Q000494:pharmacology*; D016716:PC12 Cells; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D051381:Rats; D011942:Receptors, Adrenergic, alpha / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D013879:Thioredoxins / Q000235:genetics*; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism*; D015854:Up-Regulation / Q000187:drug effects*
chemical_list: D011942:Receptors, Adrenergic, alpha; D013879:Thioredoxins; D000242:Cyclic AMP; D014446:Tyrosine 3-Monooxygenase; D019869:Phosphatidylinositol 3-Kinases; D017868:Cyclic AMP-Dependent Protein Kinases; D004837:Epinephrine
keywords: Epinephrine; Stress; Thioredoxin-1; Tyrosine hydroxylase; β-adrenergic receptor