• 2019-10
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  • 2020-08
  • cells of tissue that was inflamed owing to


    cells of tissue that was inflamed owing to H pylori infection 937
    879 mainly in gastric pits and gastric gland ductal epithelium, (Figure 7). In addition, CD44v9 expression was detected in 938
    880 but also was detected in other cell types (Figure 7A). CAPZA1-overexpressing PCI-32765 of H pylori–eradicated tissue 939
    881 Although these cell types were not identified, we showed (Figure 7A and C, case 11), suggesting that accumulation of 940
    882 that CD44v9 expression was detected in CAPZA1- CagA caused by H pylori infection contributes to induction of 941
    883 overexpressing cells in gastric epithelium with or without CD44v9 expression after eradiation therapy. These findings 942
    CAPZA1 Enhance CD44v9 Expression 9
    10 Tsugawa et al Cellular and Molecular Gastroenterology and Hepatology Vol. -, No. -
    show that analysis of CAPZA1 expression levels after erad- injects CagA via the bacterial type IV secretion system.30 1120
    ication therapy can provide important insights into the risk Injected CagA usually is degraded by autophagy.16 There- 1121
    of gastric cancer after H pylori eradication.
    fore, CagA must evade autophagic degradation to promote 1122
    These findings show that H pylori infection induces reprogramming of mucus pit cells and their de- 1123
    CD44v9 expression in CAPZA1-overexpressing cells as fol- differentiation into tissue stem-like precursor cells. We 1124
    lows: (1) overexpression of CAPZA1 enhances expression of previously reported that CAPZA1 also is overexpressed in 1125
    b-catenin, (2) overexpression of CAPZA1 induces high mucus pit cells and that CagA evades autophagic degrada- 1126
    ESRP1 expression, (3) H pylori infection of CAPZA1- tion in CAPZA1-overexpressing cells.21 Therefore, intestinal 1127
    overexpressing cells enhances nuclear translocation of transdifferentiation of gastric epithelial cells and expansion 1128
    b-catenin owing to accumulation of CagA, and (4) ESRP1 of CD44v9-positive cells are thought to occur when CAPZA1- 1129
    overexpression promotes alternative splicing of CD44total overexpressing pit cells are abundant in H pylori–infected 1130
    to generate CD44v9 (Figure 8C). By contrast, in H pylo- gastric mucosa.
    ri–infected cells not overexpressing CAPZA1, CD44v9 H PCI-32765 pylori infection induces a chronic inflammatory 1132
    expression is not induced because CagA is degraded by response by the host.28 Chronic oxidative stress is thought 1133
    autophagy, and b-catenin and ESRP1 are lowly expressed to increase the risk of gastric carcinogenesis by increasing 1134
    the level of DNA damage and by preventing DNA repair.31 1135
    Here, we showed that the levels of CAPZA1 expression and 1136
    oxidative damage in H pylori–infected gastric mucosa were 1137
    The present study makes a significant contribution to the eradication therapy is thought to decrease the level of 1139
    field of carcinogenesis in H pylori–infected gastric mucosa. CAPZA1-overexpressing cells in gastric mucosa because it 1140
    Specifically, our results show a novel and pivotal role of effectively reduces chronic inflammation caused by H py- 1141
    CAPZA1 in CD44v9 expression and show that the presence lori infection. In the present study, CAPZA1 expression was 1142
    of CAPZA1-overexpressing cells induces expansion of decreased after eradication therapy, but this effect was not 1143
    CD44v9-positive cells. The induction of CD44v9 expression significant (Figure 7B). The reason for this may be that 1144
    in CAPZA1-overexpressing cells infected with H pylori is these biopsy specimens were taken from patients with a 1145
    caused by aberrant b-catenin signaling via intracellularly mild-to-moderate level of neutrophil infiltration even after 1146
    accumulated CagA and by alternative splicing of CD44total eradication therapy. These findings suggest that continu- 1147
    via overexpression of ESRP1. Accumulation of CagA in ation of the inflammatory response after eradication 1148
    CAPZA1-overexpressing cells also aberrantly induced SALL4 therapy contributes to formation of CD44v9-positive cells 1149
    and KLF5 expression. These findings show that over- owing to survival of CAPZA1-overexpressing cells with 1150
    expression of CAPZA1, in combination with accumulation of accumulated CagA. In fact, we observed CD44v9-positive 1151
    CagA, predisposes cells to develop into CD44v9-positive cells in gastric tissues from a patient who had received