Department of

Chemical Engineering

Designing molecular technology for the 21st century with biology and chemistry

Fall 2011 Seminars

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The Interface Between Hemostasis and Inflammation:
Improving Healing by Tissue Engineering

William Velander
Department Chair and Professor
Chemical & Biomolecular Engineering
University of Nebraska–Lincoln

Thursday, September 29
10:00 a.m. - 11:00 a.m.
102 Chemistry Building

The healing process from catastrophic trauma can begin within minutes to a few hours after hemorrhage has been controlled. Immediately after regaining hemostasis, damaged tissue debridement begins by the recruitment of specialized leukocytes that will undertake proteolysis and phagocytosis at the wound site. This necessary part of the inflammation process clears cellular debris and contaminants caused by the trauma event. It optimally should take only few days to occur.

Thereafter, the recruitment and proliferation of fibroblast cells is done to generate a temporary tissue replacement (granulation tissue) that renders mechanical stability. The morbidity of serious wounds is centered about this transition and a tendency for runaway inflammation that causes systemic disruptions in hemostasis, inordinate scarring and wound contraction. Only when the inflammation phase efficiently recedes, can the recruitment and colonization of an array of progenitor cells (such as those leading to re-vascularization) be productive in its replacement of granulation tissue with a functional, more native tissue.

The treatment of hemorrhage provides a tissue engineering opportunity to guide the healing process by stemming runaway inflammation during the debridement phase and promoting an accelerated transition to a well vascularized, more functional, less scarred tissue. The proteins that play a central role in hemostasis (blood clotting) also play a key role in mitigating inflammation. We have biosynthesized abundant quantities of recombinant versions of fibrinogen, thrombin, factor XIIIa, protein C and growth factors such as FGF-1. We have further engineered kinetically fast formulations of recombinant fibrin surgical glue for the treatment of exsanguinating hemorrhage.

Our studies in pig liver surgical trauma models show that this recombinant fibrin surgical glue combined with synthetic, nanofibrous, resorbable polymeric scaffolds yield a potent hemostatic device. Importantly, these same hemostatic devices can also be used as an efficient vehicle for administration of anti-inflammatory proteins such as recombinant protein C and growth factors FGF-1 to aid healing.

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