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Hydrocortisone inhibits cellular proliferation by downregulating hepatocyte growth factor synthesis in human

Yoshihiko Tsunashima1, Ayami Kondo, Tomohiro Matsuda

  • 1Department of Pharmacology, School of Dentistry, Aichi-Gakuin University, Nagoya, Japan.

Biological & Pharmaceutical Bulletin
|May 3, 2011
PubMed

Insights

Hydrocortisone reduces osteoblast proliferation by decreasing hepatocyte growth factor (HGF) synthesis. This disruption of the HGF autocrine/paracrine loop inhibits bone cell growth, impacting bone metabolism.

Area of Science:

  • Cell Biology
  • Endocrinology
  • Bone Metabolism

Background:

  • Glucocorticoids impact bone metabolism and directly inhibit osteoblast proliferation.
  • Human osteoblasts express hepatocyte growth factor (HGF) and its receptor, c-Met.
  • The role of HGF in glucocorticoid-induced osteoblast inhibition is not fully understood.

Purpose of the Study:

  • To investigate whether hydrocortisone-induced inhibition of osteoblast proliferation is mediated by HGF.
  • To elucidate the mechanism by which hydrocortisone affects osteoblast growth.

Main Methods:

  • Utilized human osteoblastic SaM-1 cells and human osteosarcoma cell lines (HOS, SaOS-2).
  • Assessed gene and protein expression of HGF and c-Met.
  • Measured cellular proliferation in response to hydrocortisone, exogenous HGF, and a c-Met inhibitor (SU11274).

Main Results:

  • Hydrocortisone decreased HGF expression and osteoblast proliferation in SaM-1 cells in a dose-dependent manner.
  • This effect was not observed in HGF-deficient HOS and SaOS-2 cells.
  • Exogenous HGF and c-Met inhibition modulated proliferation, suggesting involvement of the HGF/c-Met pathway.

Conclusions:

  • Hydrocortisone inhibits SaM-1 cell proliferation by downregulating HGF synthesis.
  • This inhibition occurs via disruption of the autocrine/paracrine HGF signaling loop.
  • Findings highlight HGF's critical role in mediating glucocorticoid effects on osteoblasts.

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