Decreased smooth muscle function, peristaltic activity, and gastrointestinal transit in dystrophic (mdx) mice

摘要: Background Duchenne muscular dystrophy (DMD) is characterized by the lack of dystrophin in skeletal, cardiac, and smooth muscle. Slow colonic transit constipation are common DMD patients animal models DMD. However, cause this hypocontractility expression contractile proteins muscle unknown. The aim study was to investigate function colon control mdx mice. Methods Muscle contraction measured strips isolated cells. Peristaltic activity ex vivo preparations spatiotemporal mapping, gastrointestinal (GI) distribution fluorescent marker along intestine colon. mRNA smoothelin, caldesmon, calponin, tropomyosin qRT-PCR. Results Expression for decreased mice compared with control. Contraction response acetylcholine KCl cells Distension colons Krebs buffer induced peristalsis both mice; however, significantly fewer full peristaltic waves were recorded GI also inhibited Conclusion inferences data indicate that causes decrease contractility, peristalsis, provides basis analysis mechanisms involved dysfunction