Berlin 2024 – wissenschaftliches Programm
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BP: Fachverband Biologische Physik
BP 14: Poster IIa
BP 14.17: Poster
Dienstag, 19. März 2024, 18:00–20:30, Poster E
Dystrophin as a tension regulator in human skeletal muscles — •Mariam Ristau1, Arne Hofemeier1,2, Bart Vos1, Till Münker1, Mattias Luber1, and Timo Betz1 — 1Third Institute of Physics - Biophysics, Georg-August-University Göttingen — 2Institute of Pharmacology and Toxicology - University Medical Center Göttingen
Skeletal muscles are associated with contraction, movement and force generation. They are important for maintaining posture, bone and joint stability. Muscular dystrophies such as Duchenne muscular dystrophy (DMD) result in progressive weakening and wasting of skeletal muscles. DMD is caused by the loss of the protein dystrophin which is thought to stabilize and protect muscle fibres from injury.
We have studied the contractile potential of reconstituted tissues derived from healthy and DMD patients, and found that DMD derived tissues exhibited an overall weaker contractility compared to healthy derived tissues. In contrast, DMD derived tissues showed an overall higher homeostatic tissue 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 established a DMD knockout model from healthy myoblasts by using the CRISPR/Cas9 system. Comparing the healthy tissues to the isogenic DMD tissues we could reproduce the same phenotype of increased homeostatic tissue tension in the DMD tissues, providing further evidence that dystrophin may regulate homeostatic tissue tension.
Keywords: Homeostatic tissue tension; Membrane tension; Duchenne muscular dystrophy; Skeletal muscles