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Hello, everyone.
I'm Gregory Schultz, a biochemist
at the University of Florida,
and Professor of
Obstetrics and Gynecology,
and Director of the
Institute for Wound Research.
This presentation will deal with
the basic molecular and cellular
regulation of normal wound healing.
But in addition, we'll
look at what goes wrong
when wounds fail to
heal, or heal too much.
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A brief overview of the topics
that we will discuss today
includes considering wound healing
as a spectrum of outcomes, that
is normal scars, but in addition
fibrotic scars or chronic wounds.
We will begin by reviewing the
sequential phases of normal wound
healing, and I especially want to
emphasize the beneficial effects
of controlled information
and protease activities.
Because I will contrast
the beneficial effects
of controlled information
and protease activities
with the detrimental
effects on healing
that occurs when chronic
inflammation is caused
by planktonic, and
especially biofilm bacteria.
And I'll show you that these
lead to elevated levels
of protease activities, especially
the matrix metalloproteinase,
or MMPs.
Because these proteases
destroy proteins
that are essential for healing, such
as the Extracellular Matrix, or ECM
proteins, growth factors,
or their receptors.
And especially we'll also
learn about the key roles
that Transforming Growth Factor
Beta or TGFB and CTGF, or Connective
Tissue Growth Factor, play
in stimulating excessive scar
formation, or known
clinically as fibrosis.
And we'll look at
some new ways to try
to reduce pathological
scar formation.
