Characterization of the nuclear deformation caused by changes in endothelial cell shape.
We investigated the mechanotransduction pathway in endothelial cells between their nucleus and adhesions to the extracellular matrix. First, we measured nuclear deformations in response to alterations of cell shape as cells detach from a flat surface. We found that the nuclear deformation appeared to be in direct and immediate response to alterations of the cell adhesion area. The nucleus was then treated as a neo-Hookean compressible material, and we estimated the stress associated with the cytoskeleton and acting on the nucleus during cell rounding. With the obtained stress field, we estimated the magnitude of the forces deforming the nucleus. Considering the initial and final components of this adhesion-cytoskeleton-nucleus force transmission pathway, we found our estimate for the internal forces acting on the nucleus to be on the same order of magnitude as previously measured traction forces, suggesting a direct mechanical link between adhesions and the nucleus.
Jean
Ronald P
RP
Department of Biomedical Engineering, The Johns Hopkins University, Baltimore, MD 21205, USA.
Gray
Darren S
DS
Spector
Alexander A
AA
Chen
Christopher S
CS
D000818:Animals; D002417:Cattle; D002448:Cell Adhesion / Q000502:physiology; D002467:Cell Nucleus / Q000187:drug effects / Q000502:physiology* / Q000648:ultrastructure*; D048429:Cell Size / Q000187:drug effects; D002478:Cells, Cultured; D003198:Computer Simulation; D004305:Dose-Response Relationship, Drug; D004548:Elasticity; D042783:Endothelial Cells / Q000166:cytology* / Q000187:drug effects / Q000502:physiology*; D005109:Extracellular Matrix / Q000187:drug effects / Q000502:physiology / Q000648:ultrastructure; D040542:Mechanotransduction, Cellular / Q000187:drug effects / Q000502:physiology*; D008955:Models, Cardiovascular; D013314:Stress, Mechanical; D014357:Trypsin / Q000494:pharmacology*
D014357:Trypsin