Michael L. Smith

TL;DR: It is concluded that the resting state of Fn fibrils does not contain Fn molecules with crossed-over arms, and that the several-fold extensibility of Fnfibrils involves the unfolding of type III modules, which could imply that Fn might play a significant role in mechanotransduction processes.

TL;DR: The data provide the first evidence that adenosine, extracellularly formed by CD73, can modulate coronary vascular tone, inhibit platelet activation, and play an important role in leukocyte adhesion to the vascular endothelium in vivo.

TL;DR: It is concluded that leukocyte-expressed PSGL-1 serves as the main L-selectin ligand in inflamed postcapillary venules, providing a molecular mechanism for the inflammatory defects seen in L- selectin–deficient mice.

TL;DR: Fibre stretch-assay studies reveal that collagen I's Fn-binding domain is responsible for the mechano-regulated interaction and it is shown that Fn-collagen interactions are reciprocal: relaxed Fn fibrils act as multivalent templates for collagen assembly, but once assembled, collagen fibres shield Fn fibres from being stretched by cellular traction forces.

TL;DR: Fn fibers can be extended more than 8-fold (>700% strain) before 50% of the fibers break, and fiber extension steadily up-regulates fiber rigidity and cryptic epitope exposure, both of which are known to differentially alter cell behavior.