Participation of aquaporin-5, surfactant-A, endothelin-1 and telomerase in parenchymal Remodeling in experimental models of pulmonary fibrosis bleomycin-induced and 3-5-DI-TERT-4-hydroxytoluene

• Grant number: 13/06407-5
• Support Opportunities: Scholarships in Brazil - Scientific Initiation
• Start date: March 01, 2014
• End date: February 28, 2015
• Field of knowledge: Health Sciences - Medicine - Pathological Anatomy and Clinical Pathology
• Principal Investigator: Vera Luiza Capelozzi
• Grantee: Marcelo Antunes
• Host Institution: Faculdade de Medicina (FM). Universidade de São Paulo (USP). São Paulo , SP, Brazil

Abstract

Fibrosing lung diseases (FLD) are a serious problem to health and are ranked high among chronic degenerative diseases due to its morbidity. The factors triggering the development of FLD are known. Immunological, genetic and/or viral components may be present. All DPF remodel the lung architecture due to constant activation, proliferation and differentiation of fibroblasts /myofibroblasts, affecting and determining the different structures in this way, qualitative and quantitative functional changes. Certainly epithelial, vascular and matrix contribute to activation of fibroblasts /myofibroblasts with altered expression of their biomechanical properties, modulated by changes in the activity of immunomodulatory receptors that generate or disruption of normal spatial formation of these cells, contributing in the process of fibrosis. Although these cells are widely studied many aspects are still poorly understood. In the present paper we have raised the hypothesis that fibroblasts/myofibroblasts given different mechanisms of pulmonary lesion occur in experimental models of fibrosing diseases induced by bleomycin (BLM) and 3-5-di-tert-butyl-4-hydroxytoluene (BHT), which enables us to establish the remodeling process closer to the human pulmonary fibrosis. The study and comprehension of the mechanisms linked with the increase in collagen fibers, in the cells intervening in their production and in the functional analysis of pulmonary fibrosis mechanisms can contribute to understanding these fibrotic pulmonary diseases' pathogenesis.