Abstract

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    The present study investigated the effects of fluoride on endoplasmic reticulum (ER) stress (ERS) and osteoblast apoptosis in vivo. Forty-eight Wistar rats were randomly divided into four groups (12/group) and exposed to 0, 50, 100, and 150 mg/L of fluoride in drinking water for 8 weeks, respectively. Peripheral blood samples and bilateral

  • Effect of siRNA PERK on fluoride-induced osteoblastic differentiation in OS732 cells

    The purpose of this work is to study the action of fluoride on osteoblastic function through knocking down double-stranded RNA-activated protein kinase (PKR)-like ER kinase (PERK) mRNA in OS732 cells (human osteoblast-like cell line). The previous researches had demonstrated that fluoride induced endoplasmic reticulum (ER) stresses in other cells or

  • [Effects on expression of osteogenesisgene in the osteoblast with endoplasmic reticulum stress induced by fluoride].

    OBJECTIVE:  To explore the gene expressions of endoplasmic reticulum stress and differentiation in osteoblast treated by excess fluoride. METHODS:  Using primary cultured human osteoblasts for fluorosis model in vitro, apoptosis was inspected by flow cytometer, and RNA was extracted for examination of the unfolded protein response and bone differentiation genes. RESULTS:  Fluoride

  • TGF-ß1 acts as mediator in fluoride-induced autophagy in the mouse osteoblast cells.

    Highlights NaF exposure significantly decreased the proliferation rate of mouse osteoblast cells in a dose dependent manner. NaF exposure induced autophagy in the osteoblast cells with an increase in TGF-ß1 expression. Overexpression of TGF-ß1 enhanced NaF-induced autophagy. Silencing of TGF-ß1 reduced NaF-induced autophagy. Abstract It is well known that excess fluoride intake

  • Simultaneous administration of fluoride and selenite regulates proliferation and apoptosis in murine osteoblast-like MC3T3-E1 cells by altering osteoprotegerin.

    The receptor activator nuclear factor kappa-B ligand (RANKL) and its decoy receptor, osteoprotegerin (OPG), are important for maintaining the balance between bone formation and resorption. However, the regulation of microelements on these factors remains unclear. In this study, we used murine osteoblast-like MC3T3-E1 cells to examine the impact of sodium

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    As noted by the National Research Council, "[p]erhaps the single clearest effect of fluoride on the skeleton is its stimulation of osteoblast proliferation." (NRC 2006). Osteoblasts are bone-forming cells. "Stimulatory effects of fluoride on osteoblasts result in formation of osteoid, which subsequently undergoes mineralization." (Fisher RL, et al. 1989). If the new

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    The osteocyte is a type of bone cell which is increasingly believed to play an important role in repairing defects that arise in bone, thereby maintaining the bone’s structural integrity. Because osteocytes are engulfed in fluoride-rich bone mineral and help resorb the bone as part of the remodeling process, they

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    Fluoride's ability to increase the osteoid content of bone is now undisputed. Osteoid is an unmineralized tissue in bone that, in the normal bone remodeling process, ultimately becomes calcified. As some observers have noted, "[t]he main histological change induced by fluoride is the increase of osteoid volume." (Arnala 1985). One way fluoride

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