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Collagen vascular diseases associated with interstitial lung diseases

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Collagen vascular diseases associated with interstitial lung diseases

Barbara Kramer (Unbekannter Einband, Englisch)

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Beschreibung

Interstitial lung diseases (ILD) or diffuse parenchymal lung diseases (DPLD) are a heterogenous group of chronic disorders that affect the distal lung. They are largely unresponsive to any currently available therapy and lead to architectural distortion of the lung parenchyma and rapid respiratory failure. The pathogenesis of the disease is not completely understood. In some ILDs like the idiopathic pulmonary fibrosis (IPF) the initial alveolar epithelial cell injury followed by ER-stress and apoptosis of alveolar epithelial cells type II (AECII) seems to be the triggering factor. Collagen vascular diseases (CVD) are a group of immunologically mediated inflammatory disorders affecting predominantly the connective tissue and the vessels, however, quite frequently, also the lung. Especially in Polymyositis (PM), Dermatomyositis (DM) and Systemic Sclerosis (SSc), ILD determines morbidity and mortality of the disease. Autoantibody expression seems to be highly predictive for pulmonary involvement. An autoantibody frequently found in PM/DM is anti histidyl-tRNA-Synthethase (anti-HisRS), most specific autoantibodies in SSc are anti-Topoisomerase1 (anti-Topo1), anti-Topoisomerase2α (anti-Topo2α) and anti-Topoisomerase2β (anti-Topo2β). In the present project it was hypothesized that autoantibodies cause development of ILD in CVD via alveolar epithelial cell injury leading to an ER-stress and apoptotic response in AECIIs. We supposed that the binding of pathogenetic antibody directed against HisRS and topoisomerases results in a loss of function of the respective proteins, which again causes aleveolar epithelial cell injury. In order to evaluate such proposed mechanism, HisRS, Topo1, Topo2α and Topo2β were silenced via siRNA transfection in vitro in A549 cells. Furthermore, inhibition of topoisomerases was performed in vitro by treating A549 cells with topotecan and etoposide. ER-stress and apoptosis were analyzed employing Western Blot, semiquantitative RT-PCR and quantitative RT-PCR. In vitro knockdown experiments (siRNA mediated) for HisRS, Topo1, Topo2α and Topo2β did not result in ER-stress or increased apoptosis markers. On the other hand it was shown that ER-stress and apoptosis occur in A549 cells after inhibition of topoisomerases with topotecan or etoposide. Performing immunohistochemistry of lung sections of a patient with SSc associated ILD revealed ER-stress and apoptosis in AECIIs. These results suggest that autoantibodies found in CVD may contribute to the development of ILD by causing ER-stress and apoptosis in AECIIs. Weniger zeigen

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Produktinformationen

Technische Daten

Erscheinungsdatum

01.03.2017

Sprache

Englisch

EAN

9783835965423

Herausgeber

VVB Laufersweiler Verlag

Serien- oder Bandtitel

Edition Scientifique

Sonderedition

Nein

Autor

Barbara Kramer

Seitenanzahl

Einbandart

Unbekannter Einband

Buch Untertitel

- Analysis of alveolar epithelial cellular stress mechanisms.

Schlagwörter

Wissenschaft, Doktorarbeit, Uni

Thema-Inhalt

M - Medizin

Höhe

210 mm

Breite

14.6 cm

Warnhinweise und Sicherheitsinformationen

Informationen nach EU Data Act

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