Lung fibrosis is excessive scarring process resulting from chronic insults of heterogenous etiology. The major hallmark of lung fibrosis is deposition of fibrous extracellular matrix (ECM) synthetized mainly by lung myofibroblasts. The major goal of this project is analysis of interplay between myofibroblasts and altering ECM niche, using newly developed mouse model harboring myoblasts with compromized ECM-receptor signaling. This phenomena will be then studied in vitro, using human myofibroblast line and mouse primary myofibroblasts to better understand the processes regulating deposition and composition of ECM in llung fibrosis. The successful candidates will learn and utilize advanced cell-biology, molecular-biology, physiology, imaging techniques and atomic force microscopy, while developing and analyzing various mouse models.
We are seeking outstanding self-motivated candidates with master’s degree in molecular biology, physiology, biochemistry or related fields. We are offering research at a state-of-the-art equipped institute with experienced colleagues, international working environment and international collaborations.
Gregor M. et al. Mechanosensing through focal adhesion-anchored intermediate filaments. FASEB J., 28:715-29, 2014.
Schiller H.B. et al. Time- and compartment-resolved proteome profiling of the extracellular niche in lung injury and repair. Mol Syst Biol., 11:819, 2015.
Jones M.G. et al. Nanoscale dysregulation of collagen structure-function disrupts mechano-homeostasis and mediates pulmonary fibrosis. Elife, 7:e36354, 2018.
Duscher D. Mechanotransduction and fibrosis. J Biomech. 47:1997–2005, 2014.
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