Morphological analysis of the mdx rectus abdominus muscle

• Grant number: 14/10258-8
• Support Opportunities: Scholarships in Brazil - Scientific Initiation
• Start date: April 01, 2015
• End date: March 31, 2016
• Field of knowledge: Agronomical Sciences - Veterinary Medicine - Animal Pathology
• Principal Investigator: Carlos Eduardo Ambrósio
• Grantee: Felipe Augusto Rós
• Host Institution: Faculdade de Zootecnia e Engenharia de Alimentos (FZEA). Universidade de São Paulo (USP). Pirassununga , SP, Brazil

Abstract

The Duchenne Muscular Dystrophy (DMD) is the most common muscular dystrophy in humans , affecting one in every 3500 children born . The DMD is a X-linked genetic disease, caused by a mutation in the gene that encodes the protein, called dystrophin. Dystrophin is a protein that plays a role in stabilizing the muscle cell membrane against mechanical injury, and promote structural connection between the cellular components. Therefore, in the dystrophin protein absence, the patients muscles become more susceptible to severe and progressive muscle weakness that occurs due to continuous cycles of degeneration and limited regeneration. Consequently, occurs the inflammation process, replacement of muscle tissue for adipose tissue and subsequent fibrosis process. In this context, the main cause " mortis " in DMD patients befalls due the heart or respiratory failure, caused by functionality loss of the main muscles involved in these two life process. However, we believe that some muscles that not act directly in this process, may be closely linked to cardiac or respiratory failure, for example, the involvement of the rectus abdominus muscle in breathing. Among the animal models used for studies of DMD, the mdx mouse despite having a mild phenotype, is a widely animal used, due their genetic uniformit, easy handling and breeding. However, not all muscles of mdx mice exhibit morphology, biochemistry and compatible for DMD assays. In this study we hypothesized that as the rectus abdominis can increase respiratory potential, reducing end expiratory lung volume, these, if affected by DMD, may decrease the movement of the abdominal wall, and instead to help the respiratory potential to increase, this can generate a mechanical overload in the diaphragm. To generate data that contribute to the clarification of this hypothesis, we histologically analyzed the morphology of the abdominal rectus muscle of mdx with two months to elucidate the possible alteration present in this muscle. For morphological analysis, the macro and microscopic description of the rectus abdominis will be held. Microscopic analysis hematoxylin and eosin, Masson and Picrosirius Tricomio red will be used. The proposed of this work will generate an important data for scientific research broadening that involves the DMD respiratory failure. (AU)