@entity3957 causes apoptosis in XXXX pulp stem cells.

@entity1 @entity32 @entity3958 @entity522 @entity4674 @entity8186 @entity8187 @entity11624 @entity3957
INTRODUCTION: Untreated dental caries will eventually lead to @entity32 . Although much is known regarding the interaction of microbial antigens and the immunologic defense systems of pulp, many aspects of the pathogenesis of @entity11624 are not fully understood. The relationship between @entity1 pulp stem cells (HPSCs) and the pathogenesis of @entity11624 remains among the poorly understood areas. Many of the invading bacteria are known to produce considerable amounts of @entity3957 ( @entity3958 ), which causes apoptosis in some tissues. The aims of this study were to determine whether @entity3958 causes apoptosis in HPSCs and to examine its signaling pathway. METHODS: Stem cells were isolated from @entity1 dental pulp and incubated with 50 ng/mL @entity3958 for 48 hours. To detect apoptosis, the cells were analyzed by using flow cytometry. The mitochondrial signaling pathway was examined by determining mitochondrial membrane depolarization. Activation of the key apoptotic enzymes @entity8187 , @entity8186 , and @entity522 was assessed by using enzyme-linked immunosorbent assay. Release of @entity4674 from mitochondria was also determined. RESULTS: The number of apoptotic cells increased significantly with @entity3958 treatment from 1.6% to 16.3% (P < .01). Significant increases were also measured in the amounts of @entity8187 and @entity522 and in @entity4674 release (all P < .01) and in mitochondrial membrane depolarization (P < .05), whereas @entity8186 activity was not found. CONCLUSIONS: @entity3958 causes apoptosis in HPSCs by activating the mitochondrial pathway. It is suggested that @entity3958 might be one of the factors modifying the pathogenesis of @entity11624 by causing loss of viability of HPSCs through apoptosis.
