IL‐1β Induces and TGF‐β Reduces Vitamin D₃‐Induced Bone Resorption in Mouse Calvarial Bone Cells

Abstract

Bone cells produce multiple growth factors and cytokines that have effects on bone metabolism and can be incorporated into the bone matrix. The present study was designed to extend these observations by examining the interactions between transforming growth factor‐β (TGF‐β) or interleukin‐1β (IL‐1β) and bone cells in a rat long bone culture model. IL‐1β regulates several activities of the osteoblast cells derived from rat long bone explants in vitro. IL‐1β stimulated cellular proliferation and the synthesis of prostaglandin E₂ and plasminogen activator activity in the cultured cells in a dose‐dependent manner. TGF‐β is present in the bone matrix and potentially can be released during bone resorption. TGF‐β reduced basal bone resorption and inhibited vitamin D₃ [1,25(OH)₂D₃]‐induced bone resorption in rat long bone cells. These studies support the role of IL‐1β in the pathological modulation of bone cell metabolism, with regard to implication in the pathogenesis of osteoporosis by IL‐1β, and that TGF‐β is positively inhibiting the bone resorption.

• Interleukin‐1β
• Transforming growth factor‐β
• Osteoblast
• Osteoclast
• Prostaglandin E₂
• Plasminogen activator
• Vitamin D₃
• Bone resorption

Abbreviations
IL‐1β:	=	interleukin‐1β
PG:	=	prostaglandin
PGE2:	=	prostaglandin E2
TGF‐β:	=	transforming growth factor‐β