Smooth Myocytes - Tissue Functioning and Remodeling in the Circulatory and Ventilatory Systems - page 402

assembly that cause heightened cytoskeletal stiffness and traction forces. Actin
polymerization and action of nanomotors can indeed generate a stress field and
traction forces. However, in cells that bear cyclically significant stretch (e.g., cells
of heart and lung), cell reinforcement that causes cell stiffening thus progressively
impedes normal organ deformation during the functioning cycle. Hence, the
reinforcement response corresponds to an inadequate strategy. These cell types
then select the opposing compensatory mechanism. Fluidization means prompt
reduction in cytoskeleton stiffness and elevation in molecular mobility.
When they are subjected to repetitive homogeneous stretch, human airway
smooth myocytes rapidly soften, fluidize, and decrease traction force, with sub-
sequent slow recoveries [ 744 ]. After completion of a transient stretch-unstretch
maneuver of 4-s duration, the traction field quickly decays and slowly recovers. In
addition, in substrates of different stiffness, the greater the matrix stiffness, the larger
the static traction. On the other hand, cell response to dynamic traction is similar,
whatever the matrix stiffness [ 744 ]. Therefore, dynamic responses to stretch are gov-
erned by a bulk mechanism with a time scale of the order of 1 s that does not consider
changes in substrate stiffness. In addition, uni- and biaxial, isotropic stretches cause
identical fluidization responses. Whereas homogeneous stretch induces fluidization,
heterogeneous stretch induces reinforcement. Although fluidization response does
not depend on stretch homogeneity. subsequent recoveries markedly differ [ 744 ].
Cell response is influenced by the duration of transient stretch. Traction recovery
after a homogeneous biaxial stretch of 4-s duration never exceeds the prestretch
value, whereas traction recovery following a homogeneous stretch of 30-s duration
overtakes it. However, this reinforcement response disappears when homogeneous
biaxial transient stretches are applied repetitively. On the other hand, repetitive,
heterogeneous, transient stretches generate upon load removal a rapid fluidization
followed by reinforcement [ 744 ]. Other smooth myocyte types as well as human
umbilical vein endothelial cells exhibit the same behavior.
In summary, in repetitive homogeneous cell stretch, whether isotropic or not,
the fluidization response prevails. The reinforcement response to repetitive load
transients in human airway smooth myocytes occurs in the case of heterogeneous
cell deformations. Transient stretch causes [ 744 ]: (1) a quick detachment of the
myosin nanomotor from actin; (2) a transient decline in

F actin concentration; and

(3) a change in interactions among cytoskeletal proteins.

8.5 Vascular Smooth Myocytes

Vascular smooth myocytes are implicated in the maintenance of vessel wall, in the
regulation of blood pressure and flow, and response to wall damage. Mature smooth
myocytes are not terminally differentiated because they can change their phenotype.