TY - JOUR
T1 - Expression of Tyrosine Hydroxylase Gene in Cultured Hypothalamic Cells
T2 - Roles of Protein Kinase A and C
AU - Kedzierski, Wojciech
AU - Aguila-Mansilla, Nelson
AU - Kozlowski, Gerald P.
AU - Porter, John C.
PY - 1994/2
Y1 - 1994/2
N2 - Abstract: In hypothalamic cells cultured in serum‐free medium, the quantity of tyrosine hydroxylase mRNA increases after treatment with an activator of the protein kinase A pathway (8‐bromoadenosine cyclic AMP, 3‐isobutyl‐1‐methylxanthine, or forskolin) or an activator of protein kinase C (12‐O‐tetradecanoylphorbol 13‐acetate or sn‐1,2‐diacylglycerol). The tyrosine hydroxylase mRNA level decreases in the cells after inhibition of protein kinase C with calphostin C or after depletion of protein kinase C by extended phorbol ester treatment. These data suggest that both protein kinase pathways regulate tyrosine hydroxylase gene expression in hypothalamic cells. As simultaneous activation of both pathways has less than an additive effect on the tyrosine hydroxylase mRNA level, they appear to be interrelated. Compared with the rapid and dramatic increase of the tyrosine hydroxylase mRNA level in pheochromocytoma cells, activation of the protein kinase A or protein kinase C pathway in the cultured hypothalamic cells induces slow changes of a small magnitude in the amount of tyrosine hydroxylase mRNA. The slow regulation of tyrosine hydroxylase gene expression in hypothalamic dopaminergic neurons corresponds to the relatively high stability of tyrosine hydroxylase mRNA (half‐life = 14 ± 1 h) in these cells.
AB - Abstract: In hypothalamic cells cultured in serum‐free medium, the quantity of tyrosine hydroxylase mRNA increases after treatment with an activator of the protein kinase A pathway (8‐bromoadenosine cyclic AMP, 3‐isobutyl‐1‐methylxanthine, or forskolin) or an activator of protein kinase C (12‐O‐tetradecanoylphorbol 13‐acetate or sn‐1,2‐diacylglycerol). The tyrosine hydroxylase mRNA level decreases in the cells after inhibition of protein kinase C with calphostin C or after depletion of protein kinase C by extended phorbol ester treatment. These data suggest that both protein kinase pathways regulate tyrosine hydroxylase gene expression in hypothalamic cells. As simultaneous activation of both pathways has less than an additive effect on the tyrosine hydroxylase mRNA level, they appear to be interrelated. Compared with the rapid and dramatic increase of the tyrosine hydroxylase mRNA level in pheochromocytoma cells, activation of the protein kinase A or protein kinase C pathway in the cultured hypothalamic cells induces slow changes of a small magnitude in the amount of tyrosine hydroxylase mRNA. The slow regulation of tyrosine hydroxylase gene expression in hypothalamic dopaminergic neurons corresponds to the relatively high stability of tyrosine hydroxylase mRNA (half‐life = 14 ± 1 h) in these cells.
KW - Dopaminergic neurons
KW - Hypothalamus
KW - Protein kinase A
KW - Protein kinase C
KW - Tyrosine hydroxylase mRNA
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U2 - 10.1046/j.1471-4159.1994.62020431.x
DO - 10.1046/j.1471-4159.1994.62020431.x
M3 - Article
C2 - 7507513
AN - SCOPUS:0028096158
VL - 62
SP - 431
EP - 437
JO - Journal of Neurochemistry
JF - Journal of Neurochemistry
SN - 0022-3042
IS - 2
ER -