Microfluidic bioreactor for high control over fluid and reagent delivery.

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 (Serrano and Munoz-Canoves, 2017) and in aging (Leung and Wagner, 2013). We will focus on how the inflammatory, myogenic and vascular components integrate to coordinate muscle regeneration and how fibrosis develops in pathological conditions.

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.

ESR10 will use microfluidic devices to control and modulate the cellular environment with the ultimate goal to reconstruct the muscle niche in vitro.

Crucial technologies that will be used and developed are microfluidic devices to control the cellular environment. Taking advantages of EDEN material technology and expertise, the microfluidic device will be made using the most suited material (Flexdym, PDMS, PMMA,…) for the targeted applications and features.

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.
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.