Abstract
The present work is focused on examining the effect of the structurally similar dental monomers bis-GA and bis-GMA on the expression of histo-blood group antigens (HBGAs) in comparison with fibroblast vitality and proliferation. The fibroblast cell line McCoy-Plovdiv was cultivated in a serum-free medium and was treated with both monomers. Cell vitality was measured by the crystal violet test. Mitotic index and cell morphology were assessed. An immunocytochemical technique was applied to follow the expression of proliferative antigens PCNA and Ki-67 and of HBGA. The expression level of HBGA was measured by an improved pixel selection algorithm with proprietary software. The lowest concentration of 2.5 μmol/L did not significantly affect morphology, vitality, or proliferation activity. Interestingly, the quantitative analysis revealed augmented expression of HBGA B at 2.5 μmol/L. The higher concentrations of the dental monomers reduced cell vitality and mitotic indices and altered proliferative antigen expression. Bis-GA proved to be more toxic than bis-GMA and caused more prominent alterations including greater enhancement of HBGA B expression. We present novel evidence for altered expression of proliferative antigens and enhanced expression of HBGA B in fibroblasts treated with dental monomers bis-GA and bis-GMA suggesting that these substances affect cell morphology, proliferative activity, and antigenic profile.
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Abbreviations
- bis-GA:
-
2,2-bis[4-(2-hydroxy-3-acryloxypropoxy)phenyl]propane
- bis-GMA:
-
2,2-bis[4-(2-hydroxy-3-methacryloxypropoxy)phenyl]propane
- HBGA:
-
histo-blood group antigen(s)
- PCNA:
-
proliferating cell nuclear antigen
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Acknowledgments
The study was supported by grant no. 22/2004 (Medical University – Plovdiv). The authors thank Dr. M. Draganov for providing the McCoy-Plovdiv cell line and for his important methodological assistance.
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Sarafian, V.S., Uzunova, Y., Hayrabedyan, S. et al. Histo-blood group antigen expression and proliferative activity of fibroblasts treated with dental monomers. Cell Biol Toxicol 24, 27–37 (2008). https://doi.org/10.1007/s10565-007-9013-2
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DOI: https://doi.org/10.1007/s10565-007-9013-2