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      Correction: Fluoride Regulate Osteoblastic Transforming Growth Factor-β1 Signaling by Mediating Recycling of the Type I Receptor ALK5

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          Abstract

          In Fig 2, the y-axis for the graphs Runx2 and RANKL are incorrectly labeled. The axis should be labeled “Rative RNA abundance” Please see the corrected Fig 2 here. 10.1371/journal.pone.0176772.g001 Fig 2 Gene expression of Runx2, RANKL, Smad3 and ALK5 in rats treated by fluoride with or without SB431542. Rats was treated with sodium fluoride by gavage at 10 mgF-/kg.bw and 20 mgF-/kg.bw for 2 months, and half of rats in each group were injected with an ALK5 inhibitor (SB431542, 2.1 mg/kg.bw). The femurs were collected and extracted mRNA by Trizol reagent. Realtime PCR was used to analyze Runx2, RANKL, Smad3 and ALK5 expression. Results are expressed as mean± SD(n = 3). (**P < 0.01 compare with control group; aa P < 0.01, compare with two groups). In S1 File, the data for Runx2 and RANKL is incorrect. Please see the corrected S1 File here. Supporting information S1 File All raw data used for drawing result figures. (XLSX) Click here for additional data file.

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          Fluoride Regulate Osteoblastic Transforming Growth Factor-β1 Signaling by Mediating Recycling of the Type I Receptor ALK5

          This study aimed to preliminary investigate the role of activin receptor-like kinase (ALK) 5 as one of TGF-βR1 subtypes in bone turnover and osteoblastic differentiation induced by fluoride. We analyzed bone mineral density and the expression of genes related with transforming growth factor-β1(TGF-β1) signaling and bone turnover in rats treated by different concentrations of fluoride with or without SB431542 in vivo. Moreover, MTT assay, alkaline phosphatase staining, RT-PCR, immunocytochemical analysis and western blot analysis were used to detect the influence on bone marrow stem cells (BMSC) after stimulating by varying concentration of fluoride with or without SB431542 in vitro. The in vivo study showed SB431542 treatment affected bone density and gene expression of rats, which indicated TGF-β1 and ALK5 might take part in fluoride-induced bone turnover and bone formation. The in vitro study showed low concentration of fluoride improved BMSC cells viability, alkaline phosphatase activity, and osteocalcin protein expression which were inhibited by high concentration of fluoride. The gene expression of Runx2 and ALK5 in cells increased after low concentration fluoride treatment which was also inhibited by high concentration of fluoride. Fluoride treatment inhibited gene and protein expression of Samd3 (except 1 mgF-/L). Compared with fluoride treatment alone, cells differentiation was inhibited with SB431542 treatment. Moreover, the expression of Runx2, ALK5 and Smad3 were influenced by SB431542 treatment. In conclusion, this preliminary study indicated that fluoride regulated osteoblastic TGFβ1 signaling in bone turnover and cells differentiation via ALK5.
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            Author and article information

            Journal
            PLoS One
            PLoS ONE
            plos
            plosone
            PLoS ONE
            Public Library of Science (San Francisco, CA USA )
            1932-6203
            25 April 2017
            2017
            : 12
            : 4
            : e0176772
            Article
            PONE-D-17-15070
            10.1371/journal.pone.0176772
            5404841
            28441419
            b23d7776-3ff6-4b07-a58c-04660096c385
            © 2017 Yang et al

            This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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