Meet Inspiring Speakers and Experts at our 3000+ Global Conference Series Events with over 1000+ Conferences, 1000+ Symposiums
and 1000+ Workshops on Medical, Pharma, Engineering, Science, Technology and Business.

Explore and learn more about Conference Series : World's leading Event Organizer

Back

Manuela A A Ayee

University of Illinois at Chicago, USA

Title: Endothelial membrane stiffening under osmotic challenge

Biography

Biography: Manuela A A Ayee

Abstract

Cell volume regulation is a fundamental property of all mammalian cells. Numerous signaling pathways are known to be
activated by cell swelling and to contribute to cell volume homeostasis. Cellular biomechanics and membrane tension
have long been proposed to couple cell swelling to signaling pathways; however, the impact of swelling on these parameters
has yet to be fully elucidated. In this study, we utilize atomic force microscopy (AFM) under isotonic and hypotonic conditions
to measure the mechanical properties of human aortic endothelial membranes. From AFM force/displacement curves, we
obtain estimates of membrane elastic modulus, which refl ects the stiff ness of the sub-membrane cytoskeleton complex and the
force required for membrane tether formation, refl ecting membrane tension and membrane cytoskeleton attachment. We fi nd
that hypotonic swelling results in signifi cant stiff ening of the membrane region of endothelial cells, without a corresponding
change in membrane tension or membrane-cytoskeleton attachment. Furthermore, depolymerization of F-actin in the
cytoskeleton, which as expected results in a dramatic decrease in the cellular elastic modulus of both the membrane and the
deeper cytoskeleton, indicating a collapse of the cytoskeleton scaff old, does not abrogate swelling-induced stiff ening of the
membrane, instead this stiff ening is enhanced. We propose that the hypotonically induced membrane stiff ening should be
attributed to an increase in hydrostatic pressure that results from an infl ux of solutes and water into the cells. Most importantly,
our results suggest that increased hydrostatic pressure, rather than changes in membrane tension, could be responsible for
activating volume sensitive mechanisms in hypotonically swollen cells.