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eating system via the integrins on the cell's surface.
These connections act to alter the shape of the cells and
their nuclei (see Fig. 1.51), and with that, their physio-
logical properties. How do cells respond to changes in
the mechanics of their surroundings?
The response of the cells depends on the type of cells
involved, their state at the moment, and the specific
makeup of the matrix. Sometimes the cells respond by
changing shape. Other times they migrate, proliferate,
differentiate, or revise their activities more subtly. Often,
the various changes issue from the alterations in the
activity of genes. m
Information conveyed on these spring-like 'mechani-
cal molecules' travels from the matrix into the cell to
alter genetic or metabolic expression, and, if appropri-
ate, out from the cell back to the matrix:
We found that when we increased the stress applied to
the integrins (molecules that go through the cell's
membrane and link the extracellular matrix to the
internal cytoskeleton), the cells responded by becoming
stiffer and stiffer, just as whole tissues do. Furthermore,
living cells could be made stiff or flexible by varying the
prestress in the cytoskeleton by changing, for example,
the tension in contractile microfilaments? 17
The actual mechanics of the connections between the
extracellular matrix and the intracellular matrix is
generally achieved by numerous weak bonds - a kind
of Velcro® effect - rather than a few strong points of
attachment. The MFBs, with their very strong connec-
tions, would be an exception. These focal adhesion
and outside integrin bonds respond to changing condi-
tions, connecting and unconnecting rapidly at the recep-
tor sites when the cell is migrating, for instance.
Mechanically stressing the chemoreceptors on the cell's
surface - the ones involved in metabolism, as in Pert's
work - did not effectively convey force inside the cell.
This job of communicating the picture of local tension
and compression is left solely to the integrins, which
appear 'on virtually every cell type in the animal
kingdom'. 11 7
that the musculo-fascial-skeletal system as a whole
functions as a tensegrity. According to Ingber: 'Only
tensegrity, for example, can explain how every time that
you move your arm, your skin stretches, your extracel-
lular matrix extends, your cells distort, and the intercon-
nected molecules that constitute the internal framework
of the cell feel the pull - all without any breakage or
discontinuity.' 11 7 This is a very up-to-date statement of
the sentiment from The Endless Web with which we
started this chapter.
The sum total of the matrix, the receptors, and the
inner structure of the cell constitute our 'spatial' body.
Though this research definitively demonstrates its bio-
logical responsiveness, a question remains concerning
whether this system is 'conscious' in any real sense, or
whether we perceive its workings only via the neural
stretch receptors and muscle spindles arrayed through-
out the muscle and fascia of the fibrous body.
Structural intervention - of whatever sort - works
through this system as a whole, changing the mechani-
cal relations among a countless number of individual
tensegrity-linked parts, and linking our perception of
our kinesthetic self to the dynamic interaction between
cells and matrix.
Research into integrins has just begun to show us the
beginnings of 'spatial medicine' - and the importance
of spatial health:
To investigate the possibility further [researchers in my
group] developed a method to engineer cell shapes and
function. They forced living cells to take on different
shapes - spherical or flattened, round or square - by
placing them on tiny adhesive 'islands' composed of
extra-cellular matrix. Each adhesive island was
surrounded by a Teflon m -like surface to which cells could
not adhere. 116
By simply modifying the shape of the cell, they
could switch cells among different genetic programs.
Cells that were stretched and spread flat became
more likely to divide, whereas rounded cells that were
prevented from spreading activated a death program
known as apoptosis. When cells are neither too expanded
nor too hemmed in, they spend their energy neither
in dividing nor in dying. Instead they differentiated
themselves in a tissue-specific manner; capillary cells
formed hollow capillary tubes, liver cells secreted pro-
teins that the liver normally supplies to the blood, and
so on.
Thus, mechanical information apparently combines
with chemical signals to tell the cell and cytoskeleton
what to do. Very flat cells, with their cytoskeletons
stretched, sense that more cells are needed to cover the
surrounding substrate - as in wound repair - and that
cell division is necessary. Rounding and pressure indi-
cates that too many cells are competing for space on the
matrix and that cells are proliferating too much; some
must die to prevent tumor formation. In between those
two extremes, normal tissue function is established and
maintained. Understanding how this switching occurs
could lead to new approaches in cancer therapy and
tissue repair and perhaps even to the creation of artifi-
cial-tissue replacements. 11 8
This brings us to a very different picture of the rela-
tionship among biomechanics, perception, and health.
The cells do not float as independent 'islands' within
a 'dead' sea of intercellular matrix. The cells are con-
nected to and active within a responsive and actively
changing matrix, a matrix that is communicating mean-
ingfully to the cell, via many connections (see Figs 1.69B
and 1.70). The connections are linked through a tenseg-
rity geometry of the entire body, and are constantly
changing in response to the cell's activity, the body's
activity (as communicated mechanically along the trails
of the fiber matrix), and the condition of the matrix
itself. 11 8
Microtensegrity and optimal
biomechanical health
It appears that cells assemble and stabilize themselves
via tensional signaling, that they communicate with and
move through the local surroundings via integrins, and
58
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