PPG - Biologia Estrutural e Funcional
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Navegando PPG - Biologia Estrutural e Funcional por Autor "Alves, Gabriel Andrade [UNIFESP]"
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- ItemSomente MetadadadosAvaliação morfofuncional e estresse oxidativo no intestino de camundongos distróficos (mdx)(Universidade Federal de São Paulo (UNIFESP), 2014-12-17) Alves, Gabriel Andrade [UNIFESP]; Nouailhetas, Viviane Louise Andree Nouailhetas [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)Dystrophin is a component of the complex of dystrophin-associated proteins, which connects the cytoskeleton to the plasma membrane and the extracellular matrix. Their lack causes Duchenne Muscular Dystrophy (DMD), characterized by a progressive degeneration of skeletal and cardiac muscle, leading to death in patients third decade of life. Although DMD patients had gastrointestinal symptoms such as diarrhea and pseudo obstruction, little is known of the role of dystrophin in the intestinal smooth muscle (MLI). We aim to understand what is the role of dystrophin protein in MLI: structurally and functionally, muscle contraction. Specifically studied animal model (mdx mice), and assess the structure and ultrastructure of the ILM, the resistance loss of contractile response of the MLI exposed stretch, a loss of contractile response in medium without Ca2 + (essential for contraction) and recovery contractile respota with the replacement of the ion in the presence or absence of nifedipine (blocker Cav1.2b). Observe surprising resistance to loss of response during stretch despite the animal gut dystrophic have structural mucosal deficit and have demonstrated loss of muscle layer (30%) compared to the control, present degenerate mitochondria and sarcoplasmic reticulum change. The response in medium without calcium, dystrophic animals was more resistant both to the loss of contraction in medium without Ca2 +, as the recovery of contractility with replacement ion. Dystrophin has a peculiar role in MLI, different from that of skeletal muscle, because despite the visible structural deficit, there was an increase in resistance to loss of contractility stretch. The dystrophic mdx mice also presents kinetics in response to varying external impaired calcium concentration (thus probably with changes in Cav1.2b), which may help to understand symptoms present in DMD patients.