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Apoptosis-like cell death induction and aberrant fibroblast properties in human incisional hernia fascia

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10.1016/j.ajpath.2011.02.044
 
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hdl:2117/87100

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Diaz, Ramon
Quiles Pérez, María Teresa
Guillem Martí, JordiMés informacióMés informacióMés informació
López-Cano, Manuel
Huguet, Pere
Ramon-y-Cajal, Santiago
Reventós, Jaume
Armengol Carrasco, Manuel
Arbós Vilà, Maria Antonia
CovenanteeHospital Universitari Vall d'Hebron
Document typeArticle
Defense date2011-06-06
Rights accessRestricted access - publisher's policy
Attribution-NonCommercial-NoDerivs 3.0 Spain
Except where otherwise noted, content on this work is licensed under a Creative Commons license : Attribution-NonCommercial-NoDerivs 3.0 Spain
Abstract
Incisional hernia often occurs following laparotomy and can be a source of serious problems. Although there is evidence that a biological cause may underlie its development, the mechanistic link between the local tissue microenvironment and tissue rupture is lacking. In this study, we used matched tissue-based and in vitro primary cell culture systems to examine the possible involvement of fascia fibroblasts in incisional hernia pathogenesis. Fascia biopsies were collected at surgery from incisional hernia patients and non-incisional hernia controls. Tissue samples were analyzed by histology and immunoblotting methods. Fascia primary fibroblast cultures were assessed at morphological, ultrastructural, and functional levels. We document tissue and fibroblast loss coupled to caspase-3 activation and induction of apoptosis-like cell-death mechanisms in incisional hernia fascia. Alterations in cytoskeleton organization and solubility were also observed. Incisional hernia fibroblasts showed a consistent phenotype throughout early passages in vitro, which was characterized by significantly enhanced cell proliferation and migration, reduced adhesion, and altered cytoskeleton properties, as compared to non-incisional hernia fibroblasts. Moreover, incisional hernia fibroblasts displayed morphological and ultrastructural alterations compatible with autophagic processes or lysosomal dysfunction, together with enhanced sensitivity to proapoptotic challenges. Overall, these data suggest an ongoing complex interplay of cell death induction, aberrant fibroblast function, and tissue loss in incisional hernia fascia, which may significantly contribute to altered matrix maintenance and tissue rupture in vivo.
CitationDiaz, R., Quiles, M.T., Guillem-Marti, J., López-Cano, M., Huguet, P., Ramon-y-Cajal, S., Reventós, J., Armengol, M., Arbós, M.A. Apoptosis-like cell death induction and aberrant fibroblast properties in human incisional hernia fascia. "American journal of pathology", 06 Juny 2011, vol. 178, núm. 6, p. 2641-2653. 
URIhttp://hdl.handle.net/2117/87100
DOI10.1016/j.ajpath.2011.02.044
ISSN0002-9440
Publisher versionhttp://www.sciencedirect.com/science/article/pii/S0002944011002781
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  • Departament de Ciència dels Materials i Enginyeria Metal·lúrgica - Articles de revista [961]
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