Thursday, February 24, 2022
Assistant Professor Candidate:
Dr. Humberto Joca, PhD
Center for Biomedical Engineering and Technology
The University of Maryland School of Medicine
“Microtubule Mechanotransduction in Striated Muscle”
A novel mechanotransduction pathway where mechanical stress is transmitted via the microtubule (MT) network to activate NOX2-dependent ROS signals in heart, skeletal muscle, and other tissues. MTs tune cytoskeletal stiffness, which affects cytoskeletal mechanics and that mechanotransduction signaling of striated muscle. Under normal conditions, these signals act to induce Ca2+ release. Microtubules tune cytoskeletal stiffness, which affects cytoskeletal mechanics and mechanotransduction of striated muscle. In pathological conditions, such as Duchenne muscular dystrophy (DMD), alterations in the MT network (increased MT density and level of detyrosinated tubulin) stretch elicited abnormal ROS and Ca2+ signals that trigger arrhythmogenic events and facilitate muscle injury. While evidence suggests that microtubules enriched in detyrosinated tubulin regulate these processes in the possible contribution from several other tubulin modifications was lacking. Our most recent work dissects the contribution of MT acetylation to the regulation of cytoskeletal stiffness and mechano-activated ROS and Ca2+ signaling in healthy and dystrophic skeletal muscle and heart, adding to growing evidence that MTs contribute to the mechanobiology of striated muscle.
Please send an email to Dedra Jeffries (email@example.com) if you are interested in the seminar.