Tian Y.,Shenyang University |
Tian Y.,Liaoning Institute of Dental Research |
Liu J.,Shenyang University of Technology |
Bai X.,Shenyang University |
And 5 more authors.
Journal of Surgical Research | Year: 2015
Background Mandibular prognathism (MP) or skeletal class III malocclusion with a prognathic mandible is one of the most severe facial deformities. Recent work has revealed certain circulating microRNAs (miRNAs) are associated with MP, we conducted this study to characterize the miRNAs expression profile in surgically removed mandibular bone tissue in patients with MP and explored the role of miRNA regulation in the pathogenesis of MP. Methods Affymetrix GeneChip miRNA 3.0 Array was used to examine the miRNA expression in mandibular bone tissues from MP patients and control subjects. A variety of bioinformatic approaches were used to predict the target genes of the miRNAs, find the potential functions and pathways of the target genes, analyze their intersection with differentially expressed mRNAs, and establish miRNA-gene network. Results Eleven upregulated and 11 downregulated miRNAs with a fold change ≥2 and a P value <0.05 were identified in bone specimens of MP patients. A total of 3569 genes were predicted as targets of hsa-miR-10a-5p, hsa-miR-150-5p, hsa-miR-192-5p, hsa-miR-194-5p, hsa-miR-197-3p, hsa-miR-30d-5p, hsa-miR-342-5p and hsa-miR-629-5p, hsa-miR-1202, and hsa-miR-638. The target genes were predicted to be involved in biological functions and signaling pathways related to osteogenesis. Hsa-miR-30d-5p was the key node of miRNA-gene network. Conclusions Our results indicated a possible association between the differentially expressed miRNAs and MP pathogenesis, and the precise mechanisms are needed to be further validated. © 2015 Elsevier Inc. All rights reserved.
Zhang Z.,Liaoning Medical University |
Zhang Z.,Liaoning Institute of Dental Research |
Wang Z.,Liaoning Medical University |
Jia X.,Liaoning Medical University |
Li R.,Liaoning Medical University
Life Science Journal | Year: 2013
Objective As one of seed cells of the teeth tissue engineering techniques, dental pulp stem cells(DPSCs) play an important role in the study of the teeth regeneration reconstruction and tissue engineering techniques. Effects of dental papillae cells on the proliferation and differentiation of DPSCs and its mechanism remain unclear. We investigate those effects of dental papillae cells on the proliferation and differentiation of DPSCs and its mechanism of signal pathway. Methods DPSCs and dental papillae cells are cultured, the co-cultured systems of DPSCs and dental papillae cells are established. The intracellular mineralization nodes were observed after 14 d co-culture of DPSCs and dental papillae cells. The cell cycle of DPSCs was detected by flow cytometry after 7 d co-culture. The expression of dentin sialoprotein (DSP) protein was detected by Western blot after 5 d co-culture. Finally, we will detect the expression of DSP protein when the inhibitor of Notch pathway, PHI was administrated, and the expression of Notch1, Jagged1 gene and protein will be examined. Results The obvious mineralization nodules were observed in DPSCs after 14 d of co-culture. Flow cytometry results showed that stratified co-culture methods promoted the proliferation of DPSCs. The expression of DSP protein was significantly increased after 5 d of co-culture. Western blot results have showed that the expression of DSP protein was significantly decreased when PHI was administrated. RT-PCR and Western blot results have showed that the expression of Notch1, Jagged1 gene and protein was significantly decreased when PHI was administrated. Discussion Stratified co-culture of DPSCs and dental papillae cells can promote the mineralization, proliferation and differentiation of DPSCs and the expression of DSP protein. Stratified co-culture may promote the proliferation and differentiation of DPSCs by activating Notch signal pathway.
Zhao X.,Shenyang University |
Zhao X.,Central University of Costa Rica |
Zhao X.,Liaoning Institute of Dental Research |
Zhao X.,Liaoning Province Ord Diseases Translational Medicine Research Center |
And 12 more authors.
Cailiao Yanjiu Xuebao/Chinese Journal of Materials Research | Year: 2015
The in vitro biocompatibility (i.e. the cell proliferation and apoptosis of L929 cells) of 4 cast dental alloys (CoCrMo+1%Cu, CoCrMo+2%Cu, CoCrMo+3%Cu and CoCrMo) were evaluated by CCK-8 and Annexing-V/PI double marking methods to provide a biology reference in the clinical application of prosthodontics. Results show that the in vitro biocompatibility of 4 alloys decreases according to following sequence: CoCrMo+1%Cu, CoCrMo+2%Cu, CoCrMo and CoCrMo+3%Cu. However, the cytotoxicity grades of the 4 alloys are all ranked in level one, implying they are good enough in vitro biocompatibility. ©, 2015 All right reserved.
Zhao B.,Shenyang University |
Zhao B.,Liaoning Institute of Dental Research |
Zhao B.,Liaoning Province Oral Diseases Key Laboratory |
Zhao B.,Liaoning Province Oral Diseases Translation Medcicne Research Center |
And 9 more authors.
Cailiao Yanjiu Xuebao/Chinese Journal of Materials Research | Year: 2016
The in vitro biocompatibility of a novel magnesium phosphate whisker (M-PW) was evaluated by real-time cellular analysis (RTCA) and Annexin-V/PI double marking methods, and its antibacterial property was evaluated by co-culture method. Results show that the in vitro biocompatibility of the MPW decreased with the increase of M-PW in the suspensions. It possessed excellent in vitro biocompatibility for the suspensions containing 500 μg/mL or lower amount of the M-PW. It had no toxic effect on osteoblast cells for the suspension with 50 and 200 μg/mL of M-PW respectively. The antibacterial efficacy of the suspensions increased with the increasing amount of M-PW. The antibacterial efficacy against Escherichia coli and Staphylococcus aureus achieved 96.84% and 99.93% respectively for the suspension with 500 μg/mL of M-PW, demonstrating that the novel phosphorous-magnesium whisker possesses excellent antibacterial property. © All right reserved.
Zhang Y.,Fudan University |
Zhang K.,Liaoning Medical University |
Zhang K.,Liaoning Institute of Dental Research |
Ma L.,Liaoning Medical University |
And 7 more authors.
Archives of Oral Biology | Year: 2016
Objective The aim of the study was to evaluate the involvement of endoplasmic reticulum stress and intracellular calcium overload on the development of dental fluorosis. Methods We cultured and exposed rat ameloblast HAT-7 cells to various concentrations of fluoride and measured apoptosis with flow cytometry and intracellular Ca2+ changes using confocal microscopy, investigated the protein levels of GRP78, calreticulin, XBP1 and CHOP by western blotting, and their transcriptional levels with RT-PCR. We also created an in vivo model of dental fluorosis by exposing animals to various concentrations of fluoride. Subsequently, thin dental tissue slices were analyzed with H&E staining, immunohistochemical staining, and transmission electron microscopy, TUNEL assay was also performed on dental tissue slices for assessment of apoptosis. Result High fluoride concentration was associated with decreased ameloblast proliferation, elevated ameloblast apoptosis, and increased intracellular Ca2+ in vitro. The translation and transcription of the proteins associated with endoplasmic reticulum stress were significantly elevated with high concentrations of fluoride. Based on immunohistochemical staining, these proteins were also highly expressed in animals exposed to high fluoride concentrations. Histologically, we found significant fluorosis-like changes in tissues from animals exposed to high fluoride concentrations. Transmission electron microscopy cytology indicated significant apoptotic changes in tissues exposed to high concentrations of fluoride. Conclusions These results indicate that exposure to high levels of fluoride led to endoplasmic reticulum stress which induced apoptosis in cultured ameloblasts and in vivo rat model, suggesting an important role of calcium overload and endoplasmic reticulum stress triggered by high concentrations of fluoride in the development of dental fluorosis. © 2016 Elsevier Ltd. All rights reserved.