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Mesenchymal - epithelial role in the pathogenesis of drug-induced gingival hyperplasia in the Preliminary

Author: DiChangPing
Tutor: XuYan
School: Nanjing Medical University
Course: Stomatology
Keywords: Gingival hyperplasia Keratinocyte growth factor Keratinocyte growth factor receptor Monolayer culture Coculture
CLC: R781.4
Type: Master's thesis
Year: 2011
Downloads: 20
Quote: 0
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Abstract


Objective: nifedipine causes gingival hyperplasia mechanism is not clear, keratinocyte growth factor (keratinocyte growth factor, KGF) and its receptor (keratinocyte growth factor receptor, KGFR) in proliferative diseases plays a certain role. This study aimed to explore the gingival fibroblasts and epithelial cells by keratinocyte keratinocyte growth factor and its receptor pathway interactions nifedipine causes gingival hyperplasia in the development process and the possible pathogenic mechanisms. Methods: Human gingival fibroblasts (human gingival fibroblasts, HGFs) and keratinocytes (human gingival keratinocytes, HGKs), respectively, and two cell monolayer cultures co-cultured with different concentrations of nifedipine (0, 0.2, 20μg / mL) were cultured in monolayer culture and treated under the two types of cells, using the MTT assay of nifedipine on both cell proliferation in monolayer culture, semi-quantitative RT-PCR assay KGF and KGF mRNA expression levels respectively by ELISA and flow cytometry expression of KGF and KGFR. Compare monolayer culture and co-culture system after treatment with different concentrations of nifedipine altered expression of KGF and KGFR trend. Results: Different concentrations of nifedipine (0, 0.2, 20μg/mL) treatment three days on HGFs and HGKs no significant effect on proliferation. Nifedipine treatment, KGF and KGFR changing trends in monolayer culture and co-culture system is inconsistent. Gene level change trends: KGF and KGFR gene expression levels only in the co-culture system was significantly increased in a concentration-dependent manner. Protein levels change the trend: in monolayer culture conditions, only 20μg/mL nifedipine significantly increased KGF secretion; in co-culture conditions, KGF secretion by nifedipine treatment significantly increased in a dose-dependent manner. Monolayer culture conditions, HGKs of KGFR protein expression was significantly increased in a concentration-dependent manner; co-culture conditions, only 0.2μg/mL nifedipine can significantly increase HGKs of KGFR protein levels. Conclusion: epithelial - mesenchymal by KGF-KGFR pathway can regulate each other, nifedipine gingival cells can directly affect the expression of KGF and its receptor, while on the way through the KGF-KGFR indirect regulation of epithelial or connective tissue in the lead gingival hyperplasia mechanisms play a role. In vitro co-culture model and in vivo environment more similar, can be used for further study of mesenchymal - epithelial role in the occurrence of drug-induced gingival hyperplasia exact mechanism.

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CLC: > Medicine, health > Oral Sciences > Oral medicine > Periodontal disease
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