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My
name is Ira Herman.
I am a Professor of Developmental
Molecular and Chemical Biology
at the School of
Medicine, Tufts University
in Boston, Massachusetts, where I
direct the Center for Innovations
in Wound Healing Research,
and a graduate program
in Cellular and
Molecular Physiology.
Today I'll be sharing some insights
linked to dynamic reciprocity.
And how this notion of a dynamic
and reciprocal signaling network
plays pivotal roles in regulating
both the cellular responses
to injury and control
of wound healing.
And why, in the context
of non-healing wounds,
this dynamic and reciprocal
signaling between the cells
of the epidermal
compartment and the dermal
compartments, why this dynamic
reciprocity is disrupted
and actually could contribute
to, or be responsible for,
the non-healing
dynamics that are known.
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So we'll begin by
considering what might
be a simple definition of
what is dynamic reciprocity.
Then, talk about how this
paradigm could, and does,
apply well to the
notions of healing.
And then talk about the
extracellular matrix,
and how this relationship between
cells and their underlying,
or surrounding extracellular
matrix, contributes to the dynamics
in the cellular responses that
occur during reparative healing.
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So on the second
slide there is this is
original definition, as we call it.
Where did the term come from?
Actually, it doesn't really
derive from biological sciences,
but it was actually recognized and
re-coined in the context of biology
by Mina Bissell and her colleagues,
last century in the 1980s.
And it was immediately
recognized by us, and others,
that dynamic reciprocity could
be an important biological term
to help to describe the regulatory
role that the extracellular
matrix plays in modulating
cellular function.
Regardless of whether we're
talking about signals for growth,
signals for differentiation,
or the remodeling of tissues
that take place during the
development of the organism
or adult life, and
especially during disease,
and in our case, injury and repair.
