The role of ARMC5 in human cell cultures from nodules of primary macronodular adrenocortical hyperplasia (PMAH)

Mol Cell Endocrinol. 2018 Jan 15:460:36-46. doi: 10.1016/j.mce.2017.06.027. Epub 2017 Jul 1.

Abstract

The participation of aberrant receptors and intra-adrenal ACTH in hyperplastic tissue are considered mechanisms that regulate hypercortisolism in PMAH. Additionally, germline ARMC5 mutations have been described as the most frequent genetic abnormality found in patients diagnosed with PMAH. Previous functional studies analyzed ARMC5 role using H295R cells. Therefore, we investigated the role of ARMC5 in cell cultures obtained from PMAH nodules containing steroidogenic cells, aberrant receptors and intra-adrenal ACTH. ARMC5 silencing in non-mutated PMAH cell cultures decreased steroidogenesis-related genes and increased CCNE1 mRNA expression and proliferative capacity without affecting cell viability. Additionally, ARMC5 overexpression induced cell death in PMAH mutated cell cultures, thereby decreasing cell viability. We confirmed the role of ARMC5 as an important pro-apoptotic protein involved in PMAH-related steroidogenesis. We also report for the first time the involvement of ARMC5 in controlling proliferation and regulating cell cycle in PMAH cell cultures; these effects need to be explored further.

Keywords: ARMC5; Adrenocortical hyperplasia; Cell cultures (5 words); Cushing syndrome; PMAH.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adrenal Glands / metabolism*
  • Adrenal Glands / pathology*
  • Adrenocorticotropic Hormone / metabolism
  • Adrenocorticotropic Hormone / pharmacology
  • Aged
  • Armadillo Domain Proteins
  • Cells, Cultured
  • Female
  • Gene Expression Regulation / drug effects
  • Gene Silencing
  • Humans
  • Hyperplasia
  • Lipid Droplets / drug effects
  • Lipid Droplets / metabolism
  • Male
  • Middle Aged
  • Mutation / genetics
  • Pro-Opiomelanocortin / metabolism
  • Progesterone Reductase / genetics
  • Progesterone Reductase / metabolism
  • Receptor, Melanocortin, Type 2 / metabolism
  • Receptors, G-Protein-Coupled / metabolism
  • Sequence Analysis, DNA
  • Staining and Labeling
  • Steroid 17-alpha-Hydroxylase / genetics
  • Steroid 17-alpha-Hydroxylase / metabolism
  • Tumor Suppressor Proteins / genetics
  • Tumor Suppressor Proteins / metabolism*
  • Vasopressins / pharmacology

Substances

  • ARMC5 protein, human
  • Armadillo Domain Proteins
  • Receptor, Melanocortin, Type 2
  • Receptors, G-Protein-Coupled
  • Tumor Suppressor Proteins
  • Vasopressins
  • Pro-Opiomelanocortin
  • Adrenocorticotropic Hormone
  • 3 beta-hydroxysteroid dehydrogenase type II
  • Progesterone Reductase
  • CYP17A1 protein, human
  • Steroid 17-alpha-Hydroxylase