Dinâmica da angiogênese na evolução da fibrose septal hepática induzida por Capillaria hepática, em ratos

Submitted by Repositório Arca ([email protected]) on 2019-08-06T11:28:06Z No. of bitstreams: 1 license.txt: 1748 bytes, checksum: 8a4605be74aa9ea9d79846c1fba20a33 (MD5)Approved for entry into archive by Ana Maria Fiscina Sampaio ([email protected]) on 2019-08-21T17:12:41Z (GMT) No. of bitstreams: 1 license.txt: 1748 bytes, checksum: 8a4605be74aa9ea9d79846c1fba20a33 (MD5)Made available in DSpace on 2019-08-21T17:12:41Z (GMT). No. of bitstreams: 1 license.txt: 1748 bytes, checksum: 8a4605be74aa9ea9d79846c1fba20a33 (MD5) Previous issue date: 2009CAPES, FAPESB e FIOCRUZ.Universidade Federal da Bahia. Faculdade de Medicina. Salvador, BA, Brasil / Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil.Ratos infectados com o helminto Capillaria hepatica desenvolvem invariavelmente um tipo de fibrose septal que se origina em espaços porta e os conectam uns com os outros, resultando numa septação fibrosa sistematizada por todo o fígado. Vários aspectos peculiares deste interessante modelo de fibrose hepática foram estudados em nosso Laboratório, entre eles uns que demonstram a participação inicial e proeminente da angiogênese na patogenia deste processo. Os septos são vascularizados e seus vasos, venosos (portais), acabam por fazer conexão, seja através dos sinusóides, seja diretamente, com o sistema venoso hepático. Ao longo do tempo os septos fibrosos paulatinamente vão desaparecendo, seja após infecção única ou repetidas, mas alguns persistem até pelo menos 2 anos após a infecção inicial única. O presente trabalho tem o objetivo de seguir a evolução deste processo de fibrose septal ao longo do tempo, tomando como orientação a participação dos elementos vasculares e matriciais, identificando-os nos seus componentes celulares básicos, ressaltando a participação das células actina-positivas (leiomiócitos, miofibroblastos e pericitos) ao longo de um período de evolução desde poucas semanas até 1 ano a partir de uma infecção inicial e única. Espera-se que um estudo seqüencial dinâmico, envolvendo os componentes celulares fundamentais, vasculares e matriciais, participantes do processo de fibrogênese e do remodelamento, ao longo do tempo, possibilite uma melhor visão da patogenia e do significado da fibrose septal hepática.Rats infected with the hehriinth Capillaria hepatica invariably develop a process of septal fibrosis throughout the liver which originates in portal spaces, with porta-porta connections. Several aspects of this interesting model of hepatic fibrosis have been studied in our Laboratory, among them one that demonstrated an early and decisive participation of angiogenesis in pathogenesis. Septa are profusely vascularized and their branches, veins and capillaries, usually make connections with the venous system of the liver, both by means of the sinusoids, and directly with the hepatic veins. With passing time the fibrous septa gradually diminish in number and thickness, either after single or repeated infections, but some of them persist up to over a year. The present investigation represents an attempt to follow the evolution of the process of C. hepatica-ináuceá fibrosis in rats, since its earliest stages up to one year, by following the behavior of the fundamental cellular and matrix elements that are involved in fibrogenesis. Morphologic and morphometric observations were based on the behavior of actin-positive cells (leiomyocytes, pericytes and myofibroblasts), collagen and associated proteins, in relation to vascular proliferation and regression. It is hoped that this approach will shed some light for the understanding of the pathogenesis of fibrogenesis and remodeling on this particular and interesting experimental model of hepatic fibrosis

Dynamics of Capillaria-hepatica-induced hepatic septal fibrosis in rats

INTRODUCTION: The pathogenesis of septal hepatic fibrosis, induced in rats by Capillaria hepatica infection, was studied with the aid of a large collection of stored paraffin blocks, representative of the different evolutive phases of fibrosis which appeared in 100% of infected rats. METHODS: Studies were conducted involving histology, immunohistochemistry, immunofluorescence and morphometric methods, in order to observe the dynamic behavior of the cellular and matrix components of fibrosis, over a one year period of evolution. RESULTS: Observation verified that septal fibrosis originates from several portal spaces simultaneously. Its origin and progression involve blood vessel proliferation (angiogenesis), multiplication of actin-positive cells (pericytes and myofibroblasts) and progressive collagen deposition. By the end of 4-5 months, a progressive decrease in all these components was observed, when signs of regression of septal fibrosis became more evident over time. CONCLUSIONS: Besides indicating the fundamental role played by angiogenesis in the pathogenesis of fibrosis, these morphological data concerning the dynamics of this C. hepatica experimental model proved to be adequate for future investigations regarding the functional aspects of fibrosis induction, progression and regression

Dynamics of Capillaria-hepatica-induced hepatic septal fibrosis in rats

Submitted by Martha Silveira Berbert ([email protected]) on 2011-03-26T21:49:37Z No. of bitstreams: 1 Dynamics of Capillaria-hepatica-induced hepatic septal fibrosis in rats.pdf: 6251337 bytes, checksum: 12aae9eea22bd0788ba90287992a8f5d (MD5)Made available in DSpace on 2011-03-26T21:49:37Z (GMT). No. of bitstreams: 1 Dynamics of Capillaria-hepatica-induced hepatic septal fibrosis in rats.pdf: 6251337 bytes, checksum: 12aae9eea22bd0788ba90287992a8f5d (MD5) Previous issue date: 2010-11Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, BrasilGoiás Federal University. Biomedicine Departament. Jataí, GO, BrazilState University Feira de Santana. Biology Departament. Histology Laboratory. Feira de Santana, BA, BrazilINTRODUÇÃO: Um extenso material de patologia experimental arquivado em blocos de parafina, ilustrativo das diferentes fases da fibrose hepática septal, que 100% dos ratos desenvolvem em seguida uma infecção com o nematódeo Capillaria hepatica. MÉTODOS: O material foi sistematicamente estudado com métodos morfológicos e morfométricos, no sentido de se verificar o comportamento dos elementos celulares e matriciais durante a evolução da fibrose hepática septal ao longo de um período de um ano. RESULTADOS: Foi constatado que a fibrose septal se origina de vários espaços porta ao mesmo tempo, com proliferação vascular (angiogênese), multiplicação de células actino-positivas (pericitos, miofibroblastas) e progressivo depósito de colágeno. Ao fim dos 4-5 meses há uma involução regressiva de todos estes indícios morfológicos, mas com alguns septos persistindo bem evidentes até o fim de um ano. CONCLUSÕES: Além de ilustrar o papel fundamental desempenhado pela angiogênese, o modelo se mostrou adequado para futuros estudos funcionais relacionados com a indução, progressão e regressão da fibrose hepática.INTRODUCTION: The pathogenesis of septal hepatic fibrosis, induced in rats by Capillaria hepatica infection, was studied with the aid of a large collection of stored paraffin blocks, representative of the different evolutive phases of fibrosis which appeared in 100% of infected rats. METHODS: Studies were conducted involving histology, immunohistochemistry, immunofluorescence and morphometric methods, in order to observe the dynamic behavior of the cellular and matrix components of fibrosis, over a one year period of evolution. RESULTS: Observation verified that septal fibrosis originates from several portal spaces simultaneously. Its origin and progression involve blood vessel proliferation (angiogenesis), multiplication of actin-positive cells (pericytes and myofibroblasts) and progressive collagen deposition. By the end of 4-5 months, a progressive decrease in all these components was observed, when signs of regression of septal fibrosis became more evident over time. CONCLUSIONS: Besides indicating the fundamental role played by angiogenesis in the pathogenesis of fibrosis, these morphological data concerning the dynamics of this C. hepatica experimental model proved to be adequate for future investigations regarding the functional aspects of fibrosis induction, progression and regression