TY - JOUR
T1 - Expression and regulation of BCL-2 family genes in human adrenocortical adenomas in comparison with adrenal hyperplasia of Cushing's disease
AU - Ando, T.
AU - Shibata, H.
AU - Kurihara, I.
AU - Suzuki, T.
AU - Kobayashi, S.
AU - Hayashi, K.
AU - Hayashi, M.
AU - Murai, M.
AU - Saito, I.
AU - Saruta, T.
N1 - Funding Information:
This work is supported by Keio Gijuku Academic Development Funds to T.A., Grant-in Aid for encouragement of Young Scientists (A), Scientific Research from Japan Society for the Promotion of Science (No.12770620) to H.S., and by Grant-in-Aid for Research Project for Disorders of Adrenocortical Hormone Production from the Ministry of Health ant Welfare, Japan to T.S. To whom correspondence should be addressed at: Hirotaka Shibata M.D., Ph. D., Assistant Professor, Health Center and Department of Internal Medicine, School of Medicine,
PY - 2000
Y1 - 2000
N2 - The significance of increases in the expression of apoptosis-suppressing genes such as bcl-2 and mcl-1/EAT in human adrenal tumors has not yet been fully elucidated. Furthermore the roles of these genes in cell proliferation may involve interaction with steroidogenesis in the tumors via intracellular second messengers. Cyclic AMP (cAMP) caused human adrenocortical H295R cells to overexpress hCYP17 resulting in hypersecretion of cortisol. At the same time, however, expression of bcl-2, which has a cAMP response element (CRE), was not affected. Furthermore, in vivo Bcl-2 protein analysis showed its down-regulation in adrenal hyperplasia of Cushing's disease despite ACTH stimulation. Exogenous addition of glucocorticoid did not affect the expression of bcl-2 family genes. Expressions of Mcl-1/EAT and Bax did not differ markedly among human adrenal glands affected by various pathologies. In conclusion the down-regulation of Bcl-2 in Cushing's disease did not agree with no induction of this gene by cAMP in H295R cells, suggesting that expression of Bcl-2 protein was not regulated mainly by cAMP-protein kinase (PKA) pathways in human adrenal hyperplasia.
AB - The significance of increases in the expression of apoptosis-suppressing genes such as bcl-2 and mcl-1/EAT in human adrenal tumors has not yet been fully elucidated. Furthermore the roles of these genes in cell proliferation may involve interaction with steroidogenesis in the tumors via intracellular second messengers. Cyclic AMP (cAMP) caused human adrenocortical H295R cells to overexpress hCYP17 resulting in hypersecretion of cortisol. At the same time, however, expression of bcl-2, which has a cAMP response element (CRE), was not affected. Furthermore, in vivo Bcl-2 protein analysis showed its down-regulation in adrenal hyperplasia of Cushing's disease despite ACTH stimulation. Exogenous addition of glucocorticoid did not affect the expression of bcl-2 family genes. Expressions of Mcl-1/EAT and Bax did not differ markedly among human adrenal glands affected by various pathologies. In conclusion the down-regulation of Bcl-2 in Cushing's disease did not agree with no induction of this gene by cAMP in H295R cells, suggesting that expression of Bcl-2 protein was not regulated mainly by cAMP-protein kinase (PKA) pathways in human adrenal hyperplasia.
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U2 - 10.3109/07435800009048608
DO - 10.3109/07435800009048608
M3 - Article
C2 - 11196462
AN - SCOPUS:0034527242
SN - 0743-5800
VL - 26
SP - 853
EP - 859
JO - Endocrine Research
JF - Endocrine Research
IS - 4
ER -
