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Molecular and cellular regulation of wound healing; what goes wrong when wounds fail to heal or heal too much?
Other Talks in the Series: Wound Healing
Understanding poor lymphatic function and how to improve it: revisiting old facts and examining new leads to help wounds heal
- Prof. Neil Piller
- Flinders University, South Australia, Australia
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.
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.