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- W2462181024 abstract "The aim of the current study was to investigate whether Smad2 overexpression in JE cells induced alveolar bone loss, and to understand the mechanisms regulating the bone loss. A mouse line was created that used a cytokeratin 14 (K14) promoter to overexpress Smad2 in the epithelium of the transgenic mice (K14-Smad2). Micro CT radiographs (μCT) were used to assess bone loss, bone volume, and bone density. The expression of Tnfα, Il1-β, Ifγ, Rankl, and Opg were assessed by RT-PCR. Western blots were used to detect the protein levels of TNF-α and IL1-β. Tartrate-resistant acid phosphatase (TRAP) was used as a marker for osteoclasts. Wild type (WT) mice were used as controls in all steps of the current study. K14-Smad2 mice had 52.5% (±4.2) root exposed compared to 32.4%(±3.2) in the WT mice. There was a significant difference in alveolar bone volume in the K14-Smad2 mice when compared to WT mice 2.65 mm3 (±0.3) and 4.3 mm3 (±0.35) respectively. K14-Smad2 mice also had reduced bone density 696.8 mg/cc (±70) at 12 months when compared to WT mice 845.9 mg/cc(±10). The mRNA levels of Tnfα and Rankl increased by 3.26- and 2.5-fold respectively in the K14-Smad2 mice when compared to controls. The protein level of TNF-α was also significantly increased to 2.8-fold in K14-Smad2 mice when compared to WT mice. Smad2 overexpression increased the total numbers of osteoclasts in K14-Smad2 mice (3.4 ± 0.2)-fold when compared to WT mice. Smad2 overexpression induces alveolar bone loss and increases the numbers of osteoclasts. Also, Smad2 overexpression up-regulates TNF-α and RANKL." @default.
- W2462181024 created "2016-07-22" @default.
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- W2462181024 date "2016-11-01" @default.
- W2462181024 modified "2023-10-12" @default.
- W2462181024 title "Smad2 overexpression induces alveolar bone loss and up regulates TNF-α, and RANKL" @default.
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- W2462181024 doi "https://doi.org/10.1016/j.archoralbio.2016.06.023" @default.
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