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Printable Handouts
Navigable Slide Index
- Introduction
- Overview of topics
- Wound healing as a spectrum of clinical outcomes
- Molecular & cellular events in skin wound healing
- Hemostasis (Fibrin clot & platelets)
- Vascular response, blood clot & platelet response
- Cytokine & growth factor expression
- Major families of growth factors
- Inflammation
- Benefits of controlled wound inflammation
- Neutrophils & macrophages produce ROS
- Major cytokines involved in wound healing
- Repair phase
- Scar tissue replaces provisional wound matrix
- Angiogenesis (VEGF and controlled MMP activity)
- Contraction of wounds by myofibroblasts
- Epithelial healing of deep skin wounds
- Remodeling phase
- Remodeling phase (examples)
- Controlled MMPs are necessary for wound healing
- Molecular pathology of chronic wounds
- Hypothesis of chronic wound pathophysiology
- Molecular environments: healing & chronic wounds
- MMP activity in chronic wounds as wounds heal
- Protease activity predicts rate & extent of healing
- Healthy skin vs. venous ulcer tissues: MMP levels
- Percent wound closure & MMP-1 levels
- Fibronectin in non-healing vs. healing ulcers
- Fibronectin: cell attachment, spreading, migration
- PDGF-AA in normal vs. wounded skin
- TGFβR-2 in chronic venous ulcers and in healing
- Applying the principles of wound bed preparation
- Wound bed preparation and ‘TIME’
- Major developments in last 10 years
- Pathological scarring: fibrosis
- Signaling pathway in scar formation
- 2nd generation antisense oligonucleotides (ASO)
- ASO targeting CTGF reduces scarring
- Hypertrophic scar in skin
- Phase I/IIa/Ilb/llc clinical trials in skin
- ASO or vehicle treatment of incision
- Physician responses on scar appearance
- Summary
Topics Covered
- Sequence of Molecular and Cellular Events in Skin Wound Healing
- Hemostasis, Inflammation, Repair and Remodelling
- Chronic wounds
- Role of matrix metalloproteinases in wound healing
- Wound Bed Preparation and ‘T I M E’
- Pathological Scarring
- Treatments to reduce scarring
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Talk Citation
Schultz, G. (2022, October 11). Molecular and cellular regulation of wound healing; what goes wrong when wounds fail to heal or heal too much? [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved October 13, 2024, from https://doi.org/10.69645/DAVR6179.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. Gregory Schultz, Consultant: Hollister Wounder Care, Medline, Acelity; Grant/Research Support (Principal Investigator): Hollister Wound Care, Medline, Acelity, Smith & Nephew; Stock Shareholder (Self-managed): QuickMed Technologies, BioMonde
Molecular and cellular regulation of wound healing; what goes wrong when wounds fail to heal or heal too much?
A selection of talks on Cell Biology
Transcript
Please wait while the transcript is being prepared...
0:00
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.
0:27
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.
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