Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
1995-12-14
pubmed:abstractText
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0743-5800
pubmed:author
pubmed:issnType
Print
pubmed:volume
21
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
157-68
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:articleTitle
Regulation of ACTH receptor mRNA and binding sites by ACTH and angiotensin II in cultured human and bovine adrenal fasciculata cells.
pubmed:affiliation
INSERM/INRA U307, Hôpital Debrousse, Lyon, France.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't