Grants We Funded
In 2019, The Plastic Surgery Foundation (The PSF) awarded 33 investigator-initiated projects and allocated $891,274 to support the newest, clinically relevant research in plastic surgery.
The American Society of Plastic Surgeons/PSF leadership is committed to continuing to provide high levels of investigator-initiated research support to ensure that plastic surgeons have the needed research resources to be pioneers and innovators in advancing the practice of medicine.
Search The PSF database to have easy access to full-text grant abstracts from past PSF-funded research projects 2003 to present. All abstracts are the work of the Principal Investigators and were retrieved from their PSF grant applications. Several different filters may be applied to locate abstracts specific to a particular focus area, or PSF funding mechanism.
The Mechanism of eNOS Intervention in I/R Injury
Wei Wang MD
University of Nevada
Basic Research Grant
Ischemia and reperfusion (I/R) in skeletal muscle is unavoidable in many vascular and musculoskeletal traumas, in disease, and during vascular and musculoskeletal reconstructive surgeries. It can result in significant complications including muscle dysfunction and necrosis. Protecting tissue injury from I/R has been one of the goals for many years, but except for the early restoration of blood flow to the area at risk, there is little else that can be used as a protective intervention. Our recent study has shown that local intra-arterial infusion of vascular endothelial growth factor (VEGF) protein into natural blood flow of cremaster muscle during reperfusion after 4-hr warm ischemia provided a significant microvascular protection in the cremaster muscle and promoted mRNA expression of eNOS, but not inducible NOS (iNOS) and neuron NOS (nNOS) in the cremaster muscle. However, this protection was blocked by a non-selective nitric oxide synthase (NOS) inhibitor suggesting VEGF-induced microvascular protection is endothelial NOS (eNOS) dependent. It is unknown how VEGF promoting microvascular protection and eNOS expression. However, what we known is that the activity of VEGF is mainly mediated by two receptors; VEGFR-l and VEGFR-2. Both receptors are expressed mainly in endothelial cells and are essential for angiogenesis. We hypothesize that one of these receptors or both are required for VEGF to promote microvascular protection and eNOS expression. The purpose for present study is to determine the concentration ofVEGFR-1 and VEGFR-2 in the VEGF-treated cremaster muscle and to see whether the blockage of VEGFR-I or VEGFR-2 could eliminate VEGF-induced microvascular protection and eNOS upregulation. By combining physiologic, pharmacological and molecular means, the present proposal explores the microcirculatory mechanism of VEGF intervention in vivo. The potential of clinical application for using VEGF as an intervention approach may hold promise for attenuating I/R injury in the cases like replantation, free flap transfer, organ transplantation and cardiovascular surgeries, etc. More importantly, the elucidation of microvascular mechanisms of VEGF intervention will be of great value in developing future therapeutic strategies and pharmacological manipulations aimed at exploiting this protective mechanism for the treatment of patients with ischemia in the skeletal muscle.