Live observation of Endothelial to Mesenchymal Transition.

Several studies support the emerging concept that inflammation controls stem cell fate/behaviour coordinating tissue repair (Munoz-Canoves and Serrano, 2015; Tidball and Villalta, 2010) and this balance is probably skewed in patients with late phases of chronic diseases, like muscle dystrophies ((Leung and Wagner, 2013) and in aging ((Serrano and Munoz-Canoves, 2017).

We will focus on how the inflammatory, myogenic and vascular components integrate to coordinate muscle regeneration and how Endothelial to Mesenchymal Transition (EndoMT) and fibrosis develops in pathological conditions (Piera-Velazquez et al., 2016). This will allow the identification of critical cell mediators and key factors produced by them that could be exploited in the cell and pharmacological therapy of muscle diseases.

ESR13 will design a dedicated live-imaging solution based on cutting-edge technologies to study EndoMT and cell-cell interactions in controlled conditions of cell growth, maintenance and medium injection/change over a long period of time.

Preferred profile of applicants: Background in mecatronics and/or microfluidic engineering.

Leung, D.G., and Wagner, K.R. (2013). Therapeutic advances in muscular dystrophy. Annals of Neurology 74, 404–411.
Munoz-Canoves, P., and Serrano, A.L. (2015). Macrophages decide between regeneration and fibrosis in muscle. Trends Endocrinol Metab 26, 449-450.
Piera-Velazquez, S., Mendoza, F.A., and Jimenez, S.A. (2016). Endothelial to Mesenchymal Transition (EndoMT) in the Pathogenesis of Human Fibrotic Diseases. J Clin Med 5.
Serrano, A.L., and Munoz-Canoves, P. (2017). Fibrosis development in early-onset muscular dystrophies: Mechanisms and translational implications. Semin Cell Dev Biol 64, 181-190.
Tidball, J.G., and Villalta, S.A. (2010). Regulatory interactions between muscle and the immune system during muscle regeneration. Am J Physiol Regul Integr Comp Physiol 298, R1173-1187.