Gastrointestinal Tract Disorder in Natriuretic Peptide Receptor B Gene Mutant Mice

摘要: Natriuretic peptide receptor B (NPR-B), which has high affinity for C-type natriuretic (CNP) and synthesizes intracellular cGMP, may be involved in gastrointestinal tract (GIT) regulation. A mutant allele of the NPR-B-encoding gene (Npr2) is responsible phenotype short-limb dwarfism (SLW) mouse. Homozygosity this autosomal-recessive (slw/slw) leads to death before weaning because milk retention stomach intestinal distention. To elucidate relationship between CNP/NPR-B signaling GIT function, we investigated association Npr2 mutation slw/slw mice. The pylorus large intestine mutants did not respond CNP stimulation; further, they showed pyloric lumen narrowing with randomly aligned circular muscle cells. Comparison cGMP neuronal marker distribution tissues confirmed expression tissues. An Auerbach’s plexus submucosal didn’t express expressed Ca2+. In contrast, those normal mice (controls) both Sequencing revealed that causative was a 7-base deletion exon 8, resulting frameshift premature termination codon appearance. Therefore, CNP/NPR-B-signaling defect caused by an mutation. These results facilitate better understanding role motility.