ABSTRACT
Diseases such as osteoarthritis, laminopathies, and specic cancers are shown to have compromised tissue,
cellular, and nuclear mechanics, potentially interrupting normal mechanobiological processes and providing an origin point for disease progression.1-3 Osteoarthritis of cartilage and articulating joints has a multifactorial etiology resulting in part from a homeostatic imbalance in the tissue. Cartilage degradation causes an altered micromechanical environment, increasing the expression of degrading enzymes that exacerbate the disease state.4 Laminopathies specically compromise the rigidity of the nuclear envelope and are linked to premature aging and muscular dystrophy. Cancer cells actively alter their nuclear stiffness, facilitating cell mobility and metastasis,3,5 and pluripotent cells alter their nuclear structure and stiffness prior to cell lineage commitment.6 To better understand healthy and diseased or damaged tissues, and how mechanical forces applied to tissues and cells inuence individual cell nuclei, it is important to measure the mechanics (e.g., strain) in the nucleus and quantify how nuclear mechanics regulate gene expression.
