Aging can be broadly described as time dependent physiological degeneration and the progressive loss of function in living organisms. This time dependent dysfunction typically results in the onset of a plethora of human pathologies, including cancer, diabetes, cardiovascular disorders, neurodegenerative disorders, and frailty. As a result aging individuals experience changes on a physio-anatomical level: reduced energy, poor/impaired rate of wound healing, wrinkling/tissue sagging, muscle weakness, and matrix degradation. It is our goal in the Wirtz lab to tease apart some of the underlying mechanobiology involved in this inevitable process. We ask fundamental questions such as: How does the cellular dysfunction in terms of the mechanics, energetics, epigenetics, and proteomics, play a role in the overall aging process? How can we understand and manipulate the dynamic interactions and molecular crosstalk in this cellular system to impede and/or mitigate the seemingly rapid aging process? With the aid of physical and molecular characterization techniques including: high-throughput ballistic injection nanorheology (htBIN), traction force microscopy, high-throughout cell phenotyping (htCP), single & clustered cell motility, we seek to elucidate the threads connecting the complex interplay between the molecular framework and the mechanobiology involved in aging, and aging related ailments.
S.B. Khatau, D.-H. Kim, C.M. Hale, R.J. Bloom, D. Wirtz, The perinuclear actin cap in health and disease, Nucleus, 2010
C.M. Hale, A.L. Shrestha, S.B. Khatau, P.J. Stewart-Hutchinson, L. Hernandez, C.L. Stewart, D. Hodzic, D. Wirtz, Dysfunctional connections between the nucleus and the actin and microtubule networks in laminopathic models, Biophysical Journal, 2008
P.J. Stewart-Hutchinson, C.M. Hale, D. Wirtz, D. Hodzic, Structural requirements for the assembly of LINC complexes and their function in cellular mechanical stiffness, Experimental Cell Research, 2008
J.S.H. Lee, C.M. Hale, P. Panorchan, S.B. Khatau, J.P. George, C.L. Stewart, D. Hodzic, D. Wirtz, Nuclear lamin A/C deficiency induces defects in cell mechanics, polarization, and migration, Biophysical Journal, 2007