Characterization of acellular lung scaffolds derived from equine asthma model
Autor: | Ana Lídia Jacintho Delgado, Luis Vicente Franco de Oliveira, Leticia Lopes Guimarães, Renata Kelly da Palma, Maria Angélica Miglino, Andressa Daronco Cereta, Adriana Raquel de Almeida da Anunciação, Juliana Conceição Da Silva Paulino |
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Rok vydání: | 2019 |
Předmět: |
Pathology
medicine.medical_specialty Decellularization Lung biology business.industry Histology Smooth muscle hyperplasia Epithelium respiratory tract diseases Fibronectin Extracellular matrix 03 medical and health sciences 0302 clinical medicine medicine.anatomical_structure 030228 respiratory system Laminin biology.protein Medicine 030212 general & internal medicine business |
Zdroj: | Mechanisms of lung injury and repair. |
DOI: | 10.1183/13993003.congress-2019.pa599 |
Popis: | Asthma is characterized by chronic airway inflammation which induces an abnormal extracellular matrix (ECM) deposition resulting in irreversible structural lung damage. Understanding the pathyways of ECM remodeling in Asthma is important for future treatments. In this sense, acellular lung scaffolds have provided new insights into potential disease pathomechanisms, especially for chronic diseases. Therefore, the aim of this study was to characterize and to identify inthe acellular equine asthmatic lung the differences ECM components, which may lead to phenotypic differences when cells are cultured in these scaffolds. For this, the equine asthmatic bronchi were decellularized by 1% sodium dodecyl sulfate detergent by immersion. Bronchi scaffolds were assessed by Immunohistochemistry (collagen I, III, IV, laminin, and fibronectin), Scanning electron microscopy and Histology (H&E, Colloidal Iron and Picrosirius red). Histological assessment demonstrated that characteristic architecture were preserved in decellularized bronqui. Notably, the asthmatic bronqui showed a detached epithelium, subepithelium, thickening and smooth muscle hyperplasia/hypertrophy. Electron microscopy confirmed removal of cellular bodies, retained collagen and smooth muscle hyperplasia. However, the decellularized samples showed reduced collagen I and fibronectin. In conclusion we believe that the differences observed in decelularized asthmatic equine bronqui may be a result of changes in tissue-related disease or in disease-related degradation or secretion of ECM components. Moreover, future studies involving cell–ECM interactions in equine asthma model will be necessary. |
Databáze: | OpenAIRE |
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