Imunofluorescence analisys of colagen type I, III, IV and V in experimental pulmonary fibrotic model induced by Bleomicine

• Grant number: 12/07040-5
• Support Opportunities: Scholarships in Brazil - Scientific Initiation
• Effective date (Start): July 01, 2012
• Effective date (End): June 30, 2015
• Field of knowledge: Health Sciences - Medicine - Pathological Anatomy and Clinical Pathology
• Principal Investigator: Vera Luiza Capelozzi
• Grantee: Deborah Bernardo Lopes
• Host Institution: Faculdade de Medicina (FM). Universidade de São Paulo (USP). São Paulo , SP, Brazil

Abstract

Fibrosing Lung Diseases (FLD) is a serious problem to health and are ranked high among chronic degenerative diseases due to their morbidity. The factors triggering the development of FLD are not well 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 disrupt the normal spatial formation of these cells, contributing to 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, 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.(AU)

Scientific publications

(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)

MARTINS, VANESSA; TEODORO, WALCY ROSOLIA; VELOSA, ANA PAULA PEREIRA; ANDRADE, PRISCILA; FARHAT, CECILIA; FABRO, ALEXANDRE TODOROVIC; CAPELOZZI, VERA LUIZA. Butylated hydroxytoluene induces type-V collagen and overexpression of remodeling genes/proteins in experimental lung fibrosis. HISTOLOGY AND HISTOPATHOLOGY, v. 33, n. 10, p. 1111-1123, OCT 2018. (11/09181-2, 12/03543-2, 12/07040-5)

FELIX, RENATO GONCALVES; CARVALHO BOVOLATO, ANA LIVIA; COTRIM, ONDINA SILVIA; LEAO, PATRICIA DOS SANTOS; BATAH, SABRINA SETEMBRE; GOLIM, MARJORIE DE ASSIS; VELOSA, ANA PAULA; TEODORO, WALCY; MARTINS, VANESSA; CRUZ, FERNANDA FERREIRA; et al. Adipose-derived stem cells and adipose-derived stem cell-conditioned medium modulate in situ imbalance between collagen I-and collagen V-mediated IL-17 immune response recovering bleomycin pulmonary fibrosis. HISTOLOGY AND HISTOPATHOLOGY, v. 35, n. 3, p. 289-301, MAR 2020. (11/09181-2, 18/20403-6, 13/14277-4, 12/03543-2, 12/07040-5)