The relationship between vitamin D receptor gene polymorphisms and periodontitis in turkish individuals with type 2 diabetes mellitus.

Background and Aim: Vitamin D receptor (VDR) gene polymorphisms have been implicated in the pathogenesis of many diseases, such as periodontitis and diabetes mellitus (DM). The present study aimed to evaluate the distributions of VDR polymorphisms in diabetic individuals with healthy periodontium (DMH), diabetic individuals with periodontitis (DMP), nondiabetic individuals with healthy periodontium (H), and nondiabetic individuals with periodontitis (P). Material and Methods: A total of 200 individuals (DMH = 40, DMP = 60, H = 40, and P = 60) were recruited. All clinical periodontal parameters, demographical, and biochemical variables were recorded. Blood samples were collected, and genomic DNA was isolated by Purelink® Genomic DNA Mini Kit. Genotyping of VDR polymorphisms ApaI, BsmI, FokI, and TaqI were determined by real-time polymerase chain reaction (PCR) using allele-specific probes. Results: The distribution of the BsmI variant showed differences between DMH and H groups (P = 0.034). In addition, carrying the GG genotype (OR = 0.317; 95% CI = 0.126-0.797; P = 0.013) and the G allele (OR = 2.373; 95% CI = 1.203-4.681; P = 0.012) increased the risk of type 2 DM. Moreover, it was determined that the frequency of CC genotype of FokI variant was higher in DMP compared to DMH (P = 0.046). It was determined that having the CC genotype (OR = 2.706; 95% CI = 1.185-6.176; P = 0.017) and the C allele (OR = 1.917; 95% CI = 0.995-3.694; P = 0.049) increased the risk of periodontitis among diabetic individuals. No differences were detected among groups in the genotype and allele distributions of ApaI and TaqI variants (P > 0.05). Conclusions: The present study showed that the BsmI variant was a risk factor for DM among periodontally healthy individuals and the FokI variant for periodontitis among diabetic individuals.

Partial knockdown of TRF2 increase radiosensitivity of human mesenchymal stem cells.

Telomere repeat binding factor TRF2 is a member of shelterin complex with an important role in protecting and stabilizing chromosomal ends. In the present study, we investigated the effect of partial knockdown of TRF2 on radiosensitivity of telomerase immortalized human mesenchymal stem cells (hMSC-telo1), which have a higher radioresistance compared to non telomerized counterpart. Partial knockdown of the protein achieved 15-20% reduction in TRF2 protein levels. The study compared the effect of 2.5Gy radiation in two-four days after irradiation for hMSC-telo1 cells and the cells transfected with siTRF2 and null control vector. Radio-response of the cells were examined using senescence associated ß-Gal assay (ß-Gal), colony forming assay (CFU) and γ-H2AX phosphorylation. TRF2 deficiency substantially increased radiosensitivity of cells compared to controls in both proliferation and senescence assay (2.4 fold increase in ß-Gal, 1.6 fold decrease in CFU). In addition, it increased the γ-H2AX foci as revealed by both immunfluorescence and Western blot analysis. Our data suggests that partial knockdown of TRF2 in hMSC-telo1 cells cause increased γ-H2AX foci which led to fail TRF2 to protect telomeres from radiation thus TRF2 deficiency led to a 1,5-2 fold increase in the radiosensitivity of hMSC-telo1 cells through telomere destabilization.