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Effects of endogenous hypercortisolism on bone mRNA and microRNA expression in humans

Z E Belaya1, T A Grebennikova2, G A Melnichenko2

  • 1The National Research Centre for Endocrinology, ul. Dmitria Uljanova, 11, Moscow, Russia, 117036. jannabelaya@gmail.com.

Osteoporosis International : a Journal Established As Result of Cooperation Between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA
|October 6, 2017
PubMed

Insights

Glucocorticoid excess in Cushing's disease suppresses bone formation by increasing Wnt antagonists and altering microRNAs, leading to reduced osteoblast function. These factors are potential therapeutic targets for glucocorticoid-induced osteoporosis.

Area of Science:

  • Endocrinology
  • Bone Biology
  • Molecular Biology

Background:

  • Hypercortisolism in humans impairs osteoblastogenesis and function.
  • This is mediated by increased Wnt-signaling antagonists and altered microRNA levels.
  • These microRNAs influence mesenchymal stem cell commitment towards adipocytes or cartilage over osteoblasts.

Purpose of the Study:

  • To investigate bone responses to chronic glucocorticoid (GC) excess.
  • To measure mRNA and microRNA (miR) levels in bone samples from Cushing's disease (CD) patients.

Main Methods:

  • Bone samples were collected from CD patients and non-functioning pituitary adenoma (NFPA) controls during surgery.
  • Quantitative polymerase chain reactions (qPCR) were used to analyze gene and miR expression.
  • Focus was on genes and miRs involved in bone remodeling regulation.

Main Results:

  • Hypercortisolism led to downregulation of osteoblast function genes (e.g., RUNX2, COL1A1).
  • Increased expression of Wnt antagonists (Dkk1, SOST) and specific miRs suppressing osteoblastogenesis was observed.
  • Compensatory mechanisms were noted in long-term hypercortisolism, but bone formation remained suppressed.

Conclusions:

  • Endogenous GC excess suppresses bone formation via Wnt antagonists and dysregulated miRs.
  • These molecular pathways impact mesenchymal stem cell differentiation.
  • Wnt antagonists and miRs represent promising therapeutic targets for glucocorticoid-induced osteoporosis.
Keywords:
Cushing’s diseaseGlucocorticoid-induced osteoporosisSclerostinWnt-signalingmicroRNA

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