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Increased expression of CYP17 and CYP11B1 in subclinical Cushing's syndrome due to adrenal adenomas
Author(s) -
Cao Caixia,
Yang Xuecheng,
Li Li,
Sun Ruixia,
Xian Yuxin,
Lv Wenshan,
Wang Jing,
Xu Yijun,
Gao Yanyan
Publication year - 2011
Publication title -
international journal of urology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.172
H-Index - 67
eISSN - 1442-2042
pISSN - 0919-8172
DOI - 10.1111/j.1442-2042.2011.02836.x
Subject(s) - steroid 11 beta hydroxylase , messenger rna , subclinical infection , endocrinology , medicine , blot , steroid , biology , gene , biochemistry , hormone
Objectives: To determine whether steroidogenic enzyme expression is associated with the steroid secretory pattern of subclinical Cushing's syndrome (SCS) by investigating the mRNA and protein expression of CYP17 and CYP11B1 in SCS adenomas, normal adrenal cortices (NA), non‐functional adrenal adenomas (NFA) and cortisol‐producing adenomas (CPA). Methods: Total RNA and protein were extracted from 20 CPA, six SCS, 15 NFA, and eight NA. Real‐time quantitative polymerase chain reaction (PCR) and western blotting analysis were performed to determine the mRNA and protein expression of CYP17 and CYP11B1 in different tissues. The expression of CYP17 and CYP11B1 in the adrenocortical tumors was compared expression in NA. Results: Expression of both CYP11B1 and CYP17 mRNA and protein was detected in all samples tested. The expression of CYP11B1 mRNA and protein was significantly higher in the CPA group than in the other groups and was slightly higher in SCS samples compared with NA and NFA samples (all P < 0.05). There was no significant difference in CYP11B1 mRNA and protein expression between NA and NFA samples ( P > 0.05). The expression of CYP17 mRNA and protein in different tissues was similar to that of CYP11B1. Neither CYP11B1 nor CYP17 mRNA and protein expression was correlated with plasma cortisol or adrenocorticotrophin levels (all P > 0.05). Conclusions: In conclusion, CYP11B1 and CYP17 are overexpressed in subclinical CPA and their overexpression accounts for the increased production of cortisol that is characteristic of CPA.