Journal of pediatric surgery · 2007
Ncx (Enx, Hox11L.1) is required for neuronal cell death in enteric ganglia of mice.
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Aoki Taito, Jusuf Ahmad Aulia, Iitsuka Yoshinuri, Isono Kaichi, Tokuhisa Takeshi, Hatano Masahiko
Аннотация
BACKGROUND/PURPOSE: Ncx (Enx, Hox11L.1)-deficient (Ncx-/-) mice develop mega-ileo-ceco-colon with a larger number of neuronal cells in the enteric ganglia. We investigated mechanisms related to this abnormality and directed our attention to the effects on gastrointestinal tract functions.
METHODS: The number of NADPH diaphorase or cuprolinic blue-positive neuronal cells in the enteric ganglia was examined during growth of the mice. Neuronal cell death of enteric ganglia was assayed by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labeling. Function of the gastrointestinal tract was determined by measuring excretion time of the barium chloride given into the stomach.
RESULTS: The number of neuronal cells decreased in control mice older than 2 weeks, and neuronal cell death was evident in the ganglia. However, the number of neuronal cells did not decrease in Ncx-/- mice, and cell death was rare. Excretion time of barium chloride was prolonged in all Ncx-/- mice examined and was improved by the administration of an inhibitor of nitric oxide synthase.
CONCLUSIONS: Ncx participates in cell death of enteric neurons. Motor abnormality of the gastrointestinal tract in Ncx-/- mice may be attributed to the large number of neuronal cells.
METHODS: The number of NADPH diaphorase or cuprolinic blue-positive neuronal cells in the enteric ganglia was examined during growth of the mice. Neuronal cell death of enteric ganglia was assayed by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labeling. Function of the gastrointestinal tract was determined by measuring excretion time of the barium chloride given into the stomach.
RESULTS: The number of neuronal cells decreased in control mice older than 2 weeks, and neuronal cell death was evident in the ganglia. However, the number of neuronal cells did not decrease in Ncx-/- mice, and cell death was rare. Excretion time of barium chloride was prolonged in all Ncx-/- mice examined and was improved by the administration of an inhibitor of nitric oxide synthase.
CONCLUSIONS: Ncx participates in cell death of enteric neurons. Motor abnormality of the gastrointestinal tract in Ncx-/- mice may be attributed to the large number of neuronal cells.
Предметные рубрики MeSH
AnimalsAnimals, NewbornAnimals, SucklingApoptosisBarium CompoundsCaspase 3Cell CountCell LineageCell MovementChloridesColoring AgentsDisease Models, AnimalEnteric Nervous SystemEnzyme InductionGastrointestinal TransitGene Expression Regulation, DevelopmentalGenes, bcl-2Homeodomain ProteinsIn Situ Nick-End LabelingIndolesIntestine, SmallMegacolonMiceMice, KnockoutNADPH DehydrogenaseNG-Nitroarginine Methyl EsterNeural CrestNeuronsOrganometallic CompoundsProto-Oncogene Proteins c-bcl-2Staining and LabelingStomach