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ACTH Triggered Induction of Catecholamine Biosynthetic Enzymes and NPY Gene Expression in Rat Superior Cervical Ganglia (SCG) and Neuroblastoma Cells
Author(s) -
Sabban Esther Louise,
Serova Lidia,
Gueorguiev Volodia,
Cheng ShuYuan,
Shiovitz David
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1248-b
Subject(s) - medicine , endocrinology , superior cervical ganglion , tyrosine hydroxylase , corticosterone , catecholamine , gene expression , receptor , sympathoadrenal system , transfection , biology , hormone , chemistry , dopamine , gene , biochemistry
Our previous studies suggest that ACTH play a crucial role in the regulation of catecholamine (CA) biosynthetic enzymes in SCG, since its administration was as effective as immobilization stress (IMO) in increasing expression of tyrosine hydroxylase (TH) and dopamine ß‐hydroxylase (DBH) in rat SCG. Moreover IMO stress increases expression of ACTH receptors (MC2) in SCG which directly bind ACTH. We performed several experiments to examine if ACTH has a direct effect on the regulation of CA enzyme gene expression. Adrenalectomy (ADX) led to robust elevation of plasma ACTH concentrations compared to sham operated controls. Levels of TH, DBH, NPY and MC2R mRNA in SCG, determined by real‐time RT‐PCR, were also about 2‐3‐fold higher and similar to changes observed in response to a strong stressor. In the second experiment, ACTH was injected to ADX rats, in which basal ACTH levels were controlled by corticosterone pellets. Under this condition TH and DBH mRNAs were also elevated. ACTH also induced activation of TH or DBH promoter in human neuroblastoma cells of sympathoadrenal origin, transfected with constructs where these promoters control luciferase activity. NPY mRNA levels were also induced by ACTH in these cells. The results show that ACTH can increase gene expression for CA biosynthetic enzymes in SCG even without contribution of adrenal hormones, such as glucocorticoids. (Supported by NIH grant NS44218)