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Ischemia/Reperfusion Injury Project Information

Composite Tissue Preservation

Ischemic Preconditioning of Skeletal Muscle

Exogenous Protein Delivery for Endothelial Cell Protection

Composite Tissue Preservation

The long-term goal of this research is to reduce ischemia/reperfusion (I/R) injury in tissues by directly delivering adenosine triphosphate (ATP) inside cells.  Our research group has recently developed novel lipid vesicles that when perfused in tissues deliver exogenous ATP directly into cells.  At present, we are examining the mechanisms by which this novel intracellular ATP delivery system preserves cell viability, and maintains endothelial function and skeletal muscle contractile function after I/R.  The ability to supply ischemic cells with exogenous ATP makes it feasible to maintain cell homeostasis before reperfusion and thus, ameliorate the harmful effects of oxidative stress.  This type of “energy-rich therapy” may be effective in patients undergoing organ transplantation, bypass surgery or reconstructive surgery involving traumatic amputation. 


Ischemic Preconditioning of Skeletal Muscle

Ischemic preconditioning is the phenomenon whereby brief ischemic episodes render skeletal muscle resistant to subsequent ischemia.  Two windows of protection have been described: an early phase which occurs immediately after preconditioning; and a late phase which manifests itself 24 hours after preconditioning.  The long term goal of this research is to understand the intrinsic mechanisms of late phase Ischemic preconditioning in skeletal muscle and develop mimetic agents that elicit the same protective effect.  Our interest is to use these mimetic agents clinically and improve the functional outcome of dynamic myoplasty procedures such as cardiomyoplasty or neosphicters to treat fecal or urinary incontinence. 


Exogenous Protein Delivery for Endothelial Cell Protection  

The long-term goal of this research is to develop a novel technology that will allow the rapid display of protective exogenous proteins on the surface of endothelial cells.  The initial work has been focused on complement blocking proteins to protect transplanted organs from ischemia/reperfusion (I/R) injury.  Complement activation after I/R has been thought to be responsible for delayed graft function and the hastening of acute rejection in transplanted organs.  Our new technology is an alternative to gene therapy and can display exogenous proteins on the surface of endothelial cells within one hour.  We are currently evaluating the kinetics of protein display in composite tissue allografts.

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Last Updated: February 06, 2008