Wound healing is a process that is evolutionarily conserved and essential to the survival of the species. In order to close the wound and repair the tissue, the depends on the appropriate and coordinated action of the phases: inflammatory, formation of fabric and remodeling. Thus, immunomodulatory compounds have been studied in order to accelerate wound closure or minimize tissue damage. Among these compounds, the fatty acids of the omega-3 (É-3) family, due to their properties regulatory / anti-inflammatory drugs already confirmed in several studies. Searching for an alternative to evaluate the specific functions of these fatty acids in different organs or tissues, currently laboratories around the world have used as study model, transgenic mice called FAT-1, capable of producing endogenously É-3 fatty acids, from É-6 fatty acids. In studies previously conducted by our group, we demonstrated that FAT-1 mice delayed the closure of the wound and presented an increase in the production of pro-inflammatory mediators in the inflammatory phase in which the inflammation should be resolved. The imbalance of the response inflammation modulated genes associated with the structure and function of the extracellular matrix (ECM), which were evaluated by PCR array specific for wound healing. THEMEC is a three-dimensional structure consisting of a variety of macromolecules, such as fiber-forming proteins such as: collagen, fibronectin, proteoglycans, glycosaminoglycans, and proteolytic enzymes responsible for orchestrating the correct deposition and degradation of the new tissue. As a function, the MEC provides support and guidance so that cells to reach the site of interest, in addition to influencing cell proliferation and differentiation. At the same time, it mediates the blood and nutrients supply to the tissue. Therefore, understanding the MEC-cell mechanisms and the factors that influence them, such as É-3 fatty acids, the discovery of therapeutic targets or the conscious consumption of É-3, in order to favor tissue repair and minimize possible defects in wound healing. Therefore, we will evaluate, through real-time PCR, the gene expression of constituents of the MEC, as well as specific genes that had a modulation relevant, observed by the previous PCR array assay. We will quantify using the ELISA, the production of inflammatory mediators, enzymes and growth factors, in the tissues of FAT-1 and wild type (WT) mice, referring to the formation phase of fabric and remodeling, in which the MEC is produced and active.
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