AFM profiling of lesions in animal and human models of CNS demyelination
Speaker:
Matt Urbanski
Melendez-Vasquez Lab, Hunter College
Abstract
Mechanical cues delivered by the extracellular matrix, and mediated by myosin II activity, have been shown to regulate cell morphology and gene expression independent of chemical signaling.
Work from our laboratory has demonstrated that increased ECM stiffness inhibits oligodendrocyte differentiation in a myosin II-dependent manner in vitro, and that ablation of myosin II results in enhanced myelin repair in a mouse model of focal CNS demyelination. These findings suggest that changes in ECM stiffness, sensed in a myosin II dependent-manner, may contribute to the poor remeyelination observed following traumatic injury, or in disorders such as multiple sclerosis (MS).
However, the mechanical properties of injured CNS tissue have not been well characterized. In addition, most studies were performed at low spatial resolution, and do not accurately reflect the mechanical properties of tissue at the cellular level. Our recent work addresses this by using a combined atomic force microscopy (AFM) and histological approach. We have analyzed the mechanical properties of acutely and chronically demyelinated mouse brain, as well as human MS tissue, and show that acute and chronic lesions display opposite mechanical properties.
The ASRC Neuroscience Work-in-Progress Seminars consist of an hour-long presentation on research relevant to the fields of neurobiology and translational neuroscience. Talks will be given by senior Ph.D. students, postdoctoral and faculty researchers. Anyone interested is encouraged to attend and actively participate in discussions.
Work-in-Progress Seminars are presented in collaboration with The City College of New York.