SKM 2023 – scientific programme
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BP: Fachverband Biologische Physik
BP 28: Poster Session II
BP 28.23: Poster
Thursday, March 30, 2023, 18:00–20:00, P2/EG
Dystrophin as a tension regulator in human skeletal muscles — •Mariam Ristau1, Arne Hofemeier1,2, and Timo Betz1 — 1Third Institute of Physics - Biophysics, Georg-August-University Göttingen, Germany — 2ZMBE - Institute of Cell Biology, University of Münster, Germany
Skeletal muscles are associated with contraction, movement and force generation. They are important for maintaining posture and maintaining bone and joint stability. Muscular dystrophies such as Duchenne muscular dystrophy (DMD) result in progressive weakening of skeletal muscles. DMD is caused by the loss of the protein dystrophin which is thought to stabilize and protect muscle fibers from injury. In the progression of the disease, damaged muscle fibers degrade, muscle mass is lost and greater functional impairments develop. We have studied the contractile potential of myoblasts and reconstituted tissue derived from healthy and DMD patients, and found that they were mechanically different in muscle tension and contractility. DMD derived myoblasts exhibited an overall weaker contractility compared to healthy derived myoblasts. In contrast, DMD derived myoblasts showed an overall higher muscle tension, suggesting that dystrophin may function as a tension regulator in skeletal muscles. In order to rule out the possibility that these findings are due to patient variability we intend to establish a genetic model in which we knockout dystrophin with the CRISPR/Cas9 system in healthy myoblasts and rescue dystrophin in DMD myoblasts by integrating micro-dystrophins(μDys).