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Inhibition of replication of normal adrenocortical cells in culture by adrenocorticotropin.
Author(s) -
J. Ramachandran,
A T Suyama
Publication year - 1975
Publication title -
proceedings of the national academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.72.1.113
Subject(s) - endocrinology , medicine , adrenocorticotropic hormone , dna synthesis , corticosterone , zona fasciculata , stimulation , acth receptor , biology , adrenal gland , adrenal cortex , bucladesine , cell culture , thymidine , chemistry , hormone , in vitro , biochemistry , genetics
Adrenocorticotropic hormone (ACTH) inhibited [3H]thymidine incorporation in normal adrenocortical cells of adult rats in culture, with a concomitant increase in corticosterone production and a characteristic retraction of cells. Both dibutyryl cyclic AMP and an analog of ACTH, which produces virtually no cyclic AMP, inhibited DNA synthesis and stimulated steroid production. ACTH inhibited the proliferation of adrenocortical cells obtained from suckling rats as well as the cells obtained from the capsular tissue of adult rat adrenal glands, whereas insulin caused a stimulation of DNA synthesis. These results suggest that the major role of ACTH is to induce the transformation of the undifferentiated cells of the adrenal gland into functional fasciculata cells and that the proliferation of adrenocortical cells may be under control of factors other than ACTH.

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