Expression of P-450(c11beta) in adrenal aldosterone-producing adenomas and nodular hyperplasia tissues

Clin Lab. 2011;57(3-4):245-51.

Abstract

Background: Our previous study suggests that decreased P-450(c17alpha) expression correlated with the overproduction of aldosterone in APA and nodular hyperplasia in patients with primary aldosteronism. This study was performed to further investigate if P-450(c11beta) contributes to the overproduction of aldosterone in APA and nodular hyperplasia tissues.

Methods: Total RNA and protein were extracted from 7 cases of APA tissue, 3 nodular hyperplasia tissues, 7 normal adrenal glands. P-450(c11beta) mRNA was examined by dot blot and confirmed by Northern blot analysis and by realtime PCR. Protein expression level of P-450(c11beta) was also investigated by immunohistochemical staining and confirmed by Western blot.

Results: The relative expression level of P-450(c11beta) mRNA to beta-actin in APA, nodular hyperplasia and the normal adrenal gland group are 47 +/- 22%, 55 +/- 13%, 64 +/- 16% respectively by dot blot and are 94 +/- 18%, 101 +/- 20%, 112 +/- 62% respectively by Northern blot. These results are further confirmed by realtime PCR. This result was also supported by the relative protein expression level of P-450(c11beta) to beta-actin which are 118 +/- 15%, 107 +/- 32%, 108 +/- 22% respectively evaluated by Western blot. There was no significant difference in protein expression level of P-450(c11beta) among the normal adrenal gland tissues, APA and adrenal nodular hyperplasia tissue, either (P > 0.05).

Conclusions: These results suggest that P-450(c11beta) is not a key contributor to the overproduction of aldosterone in APA and nodular hyperplasia and can not be considered as a potential marker to differentiate between them in patients with primary aldosteronism.

MeSH terms

  • Adenoma / physiopathology*
  • Adrenal Gland Neoplasms / physiopathology*
  • Adult
  • Biomarkers / metabolism
  • Blotting, Western
  • Female
  • Gene Expression Regulation, Neoplastic*
  • Humans
  • Hyperplasia / physiopathology*
  • Male
  • RNA, Messenger / metabolism
  • Reverse Transcriptase Polymerase Chain Reaction
  • Steroid 11-beta-Hydroxylase / genetics
  • Steroid 11-beta-Hydroxylase / metabolism*
  • Young Adult

Substances

  • Biomarkers
  • RNA, Messenger
  • Steroid 11-beta-Hydroxylase