Reference : Regulation of ACTH receptor mRNA and binding sites by ACTH and angiotensin II in cult...
Scientific journals : Article
Human health sciences : Endocrinology, metabolism & nutrition
Regulation of ACTH receptor mRNA and binding sites by ACTH and angiotensin II in cultured human and bovine adrenal fasciculata cells.
Penhoat, A. [> >]
LEBRETHON, Marie-Christine mailto [Centre Hospitalier Universitaire de Liège - CHU > > Pédiatrie >]
Begeot, M. [> >]
Saez, J. M. [> >]
Endocrine Research
Yes (verified by ORBi)
[en] Adrenocorticotropic Hormone/pharmacology ; Angiotensin II/pharmacology ; Animals ; Binding Sites ; Cattle ; Cells, Cultured ; Humans ; RNA, Messenger/drug effects ; Receptors, Corticotropin/analysis/drug effects/genetics ; Zona Fasciculata/chemistry/cytology/drug effects ; Zona Reticularis/chemistry/cytology/drug effects
[en] Human (HAC) and bovine (BAC) adrenal fasciculata cells express ACTH and angiotensin-II (A-II) receptors. In the present work, we have studied the effects of both hormones on ACTH receptor (ACTH-R) mRNA and binding sites. Both HAC and BAC expressed several ACTH-R transcripts. Although in both cell types, ACTH and A-II increased ACTH-R transcripts in a time- and dose-dependent manner, the maximal effects were different. Thus, ACTH at 10(-9) M enhanced 21- and 5-fold the level of ACTH-R mRNA and binding sites in HAC, whereas in BAC both parameters were enhanced only 3-fold. A-II at 10(-7) M increased 17- and 3.5-fold ACTH-R mRNA and binding sites in HAC, whereas in BAC, it caused only a 2-fold increase in ACTH-R mRNA and a small decrease in receptor number. In HAC, the stimulatory effects of both hormones on ACTH-R mRNA are mainly transcriptional, whereas in BAC they are mainly post-transcriptional, by decreasing the rate of degradation of ACTH-R mRNA. The stimulatory effects of ACTH on ACTH-R in both HAC and BAC were associated with an enhanced steroidogenic response to further hormonal stimulation. In contrast, specific species differences were observed with A-II. Thus, in HAC A-II increased ACTH-R mRNA and binding sites and the ACTH-induced cortisol production, whereas in BAC, A-II caused a slight decrease of ACTH binding sites and steroidogenic desensitization.

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