Stimulation of Mesenchymal-epithelial Transition Factor (c-Met) Expression in Candida Albicans-infected Human Gingival Epithelial Cells and Rat Gingival Epithelium
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概要
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Oral epithelial cells significantly influence host inflammatory responses against Candida albicans. Pro-inflammatory cytokines function as an early innate immune system mediator during C. albicans infection in oral epithelial cells. The presence of yeasts in periodontal pockets is well known and C. albicans is the species most commonly isolated from the oral cavity. To elucidate the molecular mechanisms governing the human gingival epithelial cells to C. albicans infection, human gingival epithelial cells (HGE) were primarily cultured and infected with C. albicans ATCC90029. Total RNA was extracted from HGE after 8 hrs of infection and monitored mRNA levels using Affymetrix GeneChip (Human Genome U133 plus 2.0 Array, 48,000 genes). GeneChip data was analyzed by GeneSpring software. The mesenchymal-epithelial transition factor (c-Met), showed a greater than 2-fold change in expression relative to those in control cells. In contrast, hepatocyte growth factor (HGF) showed an absent of gene expression in HGF. Altered mRNA levels of c-Met in GeneChip analysis were confirmed by reverse transcription polymerase chain reaction (RT-PCR) and real-time RT-PCR. Stronger immunoreactivity against c-Met was observed in the infection with C. albicans by using an in vivo rat animal model. These findings suggest that the enhanced c-Met expression is involved in the growth of gingival epithelial cells in response to C. albicans.
著者
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Kuboyama Noboru
Department Of Oral Molecular Pharmacology Nihon University School Of Dentistry At Matsudo
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Abiko Yoshimitsu
Department Of Biochemistry And Molecular Biochemistry Nihon University School Of Dentistry At Matsud
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Ohmori Jotaro
Departments of Biochemistry and Molecular Biology, Nihon University School of Dentistry at Matsudo
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Ikuta Tonami
Departments of Biochemistry and Molecular Biology, Nihon University School of Dentistry at Matsudo
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