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Fluoride induces apoptosis and alters collagen I expression in rat osteoblasts.

Authors: Yan, X  Yan, X  Morrison, A  Han, T  Chen, Q  Li, J  Wang, J 
Citation: Yan X, etal., Toxicol Lett. 2011 Feb 5;200(3):133-8. doi: 10.1016/j.toxlet.2010.11.005. Epub 2010 Nov 18.
Pubmed: (View Article at PubMed) PMID:21093551
DOI: Full-text: DOI:10.1016/j.toxlet.2010.11.005

In this study we investigated apoptosis and expression of the collagen I gene in newborn rat osteoblasts (OB) by the administration of varying concentrations of fluoride (F). Sodium fluoride (NaF) at concentrations of 0, 0.5, 5, 10, and 20mg/L was administered to cultured OB. The percentage of G(1)/G(0) (Gap 1/Gap 0), S (synthesis), G(2)/M (Gap 2/M, mitosis), and apoptosis rates in OB were analyzed with a Fluorescence-activated Cell Sorter (FACS) by propidium iodine (PI) staining after F treatment of 72 h. Effects of F treatment on COL1A1 and COL1A2 mRNA and collagen I protein levels were determined using quantitative real time RT-PCR (qRT-PCR) and immunofluorescence, respectively. This study demonstrates that there is a pronounced negative effect of long term NaF treatment on OB survival. These negative effects include an inhibition of the transformation from S phase into G(2)/M phase, increased apoptosis, and decreased COL1A1 mRNA, down-regulating the synthesis of COL I protein. The results suggest that COL I protein degradation in OB from F toxicity is due to a depletion of COL1A1 mRNA and not COL1A2.


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RGD Object Information
RGD ID: 8552690
Created: 2014-04-25
Species: All species
Last Modified: 2014-04-25
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.