## Abstract A major cellular event in vascular calcification is the phenotypic transformation of vascular smooth muscle cells (VSMCs) into osteoblast‐like cells. After demonstrating that lanthanum chloride (LaCl~3~) suppresses hydrogen peroxide‐enhanced calcification in rat calcifying vascular cell
Lanthanum enhances in vitro osteoblast differentiation via pertussis toxin-sensitive gi protein and ERK signaling pathway
✍ Scribed by Xi Wang; Lan Yuan; Jian Huang; Tian-Lan Zhang; Kui Wang
- Publisher
- John Wiley and Sons
- Year
- 2008
- Tongue
- English
- Weight
- 652 KB
- Volume
- 105
- Category
- Article
- ISSN
- 0730-2312
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✦ Synopsis
Abstract
Converging lines of evidence suggest that lanthanum tends to deposit in bone. The influence of lanthanum ion (La^3+^) on osteoblast differentiation and the related mechanism are essential to understanding its effect on bone metabolism. In this study, La^3+^ treatment enhanced in vitro osteoblast differentiation as evidenced by promoting alkaline phosphatase (ALP) activity, osteocalcin (OC) secretion, and matrix mineralization. The expressions of osteoblast‐specific genes of Cbfa‐1, osteopontin (OPN), and bone sialoprotein (BSP) were all increased in the presence of La^3+^, but no change was observed in that of type I collagen (COL‐I). Further studies demonstrated that La^3+^ treatment enhanced phosphorylation of extracellular signal‐regulated kinase (ERK). Inhibition of ERK activation by U0126 suppressed the effects of La^3+^ on osteoblast activity. Moreover, pretreatment of the cells with pertussis toxin (PTx), a Gi protein inhibitor, suppressed the La^3+^‐enhanced ERK phosphorylation and osteoblast differentiation. These findings suggest that La^3+^ exposure enhances in vitro osteoblast differentiation and the effect depends on ERK phosphorylation via PTx‐sensitive Gi protein signaling. J. Cell. Biochem. 105: 1307–1315, 2008. © 2008 Wiley‐Liss, Inc.
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