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A comparative immuno-histoquemical fibrotic study in keloid, lobomycosis and scleoderma


Fibrosis is defined defined as excess deposition of components of the extracellular matrix (ECM), especially collagen. Regardless of the etiology, fibrotic disorders have, in common, persistence of the stimulus and consequent production of growth factors, fibrogenic cytokines and angiogenic factors that stimulate the deposition of ECM components, causing remodeling and destruction of the normal tissue architecture. Chronic inflammations of varied etiologies, for example, are potent promoters of extracellular matrix formation. Recently, the cellular sources responsible for fibrosis have been highlighted: Fibroblast (Myofibroblast) Resident; Transition Mesenchymal epithelium (differentiation of cells of epithelial origin in mesenchymal phenotype cells; Monocyte-macrophages heterogeneity and Hedgehog signaling pathway (Hh): Thus, the objective of this work is to investigate common aspects of fibrogenesis in three distinct cutaneous diseases: queloid (n=20), lobomycosis (n = 20), and scleroderma (n = 20). All samples will come from the Dermatopathology Laboratory of the Hospital das Clínicas FMUSP, which were obtained for diagnostic purposes of the respective diseases or products (n = 20) will be composed of skin samples from the margins of resection of cutaneous neoplasms. Qualitative and quantitative analyzes of collagen deposition will be performed by correlating them the tissue cellular markers proposed using immunohistochemistry namely: (1) alpha-actin (smooth muscle actin); (2) collagen type 1 (col1); (3) vimentin; (4) fibroblast-specific protein 1 (FSP1); (5) cytokeratins.Key words: lobomycosis, keloid, scleroderma, fibrogenesis markers, extracellular matrix, immunohistochemistry (AU)

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