Abstract
BackgroundHeat shock protein 22 (HSP22) belongs to class I of the small HSP family that displays ubiquitous expression in osteoblasts. We previously demonstrated that prostaglandin F2α (PGF2α), a potent bone remodeling factor, induces the synthesis of interleukin-6 (IL-6) and vascular endothelial growth factor (VEGF) via p44/p42 mitogen-activated protein (MAP) kinase and p38 MAP kinase in osteoblast-like MC3T3-E1 cells. In the present study, we investigated whether HSP22 is implicated in the PGF2α-induced synthesis of IL-6 and VEGF and the mechanism of MC3T3-E1 cells.MethodsMC3T3-E1 cells were transfected with HSP22-siRNA. IL-6 and VEGF release was assessed by ELISA. Phosphorylation of p44/p42 MAP kinase and p38 MAP kinase was detected by Western blotting.ResultsThe PGF2α-induced release of IL-6 in HSP22 knockdown cells was significantly suppressed compared with that in the control cells. HSP22 knockdown also reduced the VEGF release by PGF2α. Phosphorylation of p44/p42 MAP kinase and p38 MAP kinase was attenuated by HSP22 downregulation.ConclusionsOur results strongly suggest that HSP22 acts as a positive regulator in the PGF2α-induced synthesis of IL-6 and VEGF in osteoblasts.
Highlights
Bone tissue is continuously remodeled to maintain bone homeostasis through bone remodeling, and the bone metabolism is tightly coordinated by two types of functional cells, osteoclasts and osteoblasts [1]
Regarding the intracellular signaling of prostaglandin F2α (PGF2α), we demonstrated that p44/p42 mitogen-activated protein (MAP) kinase and p38 MAP kinase are involved in the synthesis of IL-6 and vascular endothelial growth factor (VEGF) in these cells [8, 10,11,12]
Effect of PGF2α-on the IL-6 release in Heat shock protein 22 (HSP22)-knockdown MC3T3-E1 cells In our previous study, we have shown that PGF2α induces the IL-6 synthesis in osteoblast-like MC3T3-E1
Summary
Bone tissue is continuously remodeled to maintain bone homeostasis through bone remodeling, and the bone metabolism is tightly coordinated by two types of functional cells, osteoclasts and osteoblasts [1]. Regarding the intracellular signaling of PGF2α, we demonstrated that p44/p42 mitogen-activated protein (MAP) kinase and p38 MAP kinase are involved in the synthesis of IL-6 and VEGF in these cells [8, 10,11,12]. We previously demonstrated that prostaglandin F2α (PGF2α), a potent bone remodeling factor, induces the synthesis of interleukin-6 (IL-6) and vascular endothelial growth factor (VEGF) via p44/p42 mitogen-activated protein (MAP) kinase and p38 MAP kinase in osteoblast-like MC3T3-E1 cells. We investigated whether HSP22 is implicated in the PGF2α-induced synthesis of IL-6 and VEGF and the mechanism of MC3T3-E1 cells
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