The Plastic Surgery Foundation
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Grants We Funded

Grant applicants for the 2022 cycle requested a total of over $2.9 million dollars. The PSF Study Section subcommittees of Basic & Translational Research and Clinical Research evaluated 115 grant applications on the following topics:

The PSF awarded research grants totaling almost $550,000 to support 19 plastic surgery research proposals.

ASPS/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.

Research Abstracts

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.

Role of Toll-Receptor Adenosine Signalling in Wound Repair

Principal Investigator
Lisa Jacob MD


New Jersey Medical School

Funding Mechanism
Basic Research Grant

Focus Area

Macrophages play a key role in wound repair and fibroproliferative diseases by regulating fibroblast proliferation, connective tissue synthesis and angiogenesis. Macrophages produce angiogenic factors, of which Vascular Endothelial Growth Factor (VEGF) is a major component, in an exquisitely magnified manner. It has been shown recently in Dr. Leibovich's lab here at UMDNJ, that VEGF expression is strongly and synergistically regulated by an interaction between Toll-like receptor (TLR) agonists and agonists of adenosine A2A receptors (A2ARs). TLR agonists are products of micro-organisms, such as endotoxin (LPS). Adenosine is produced as a result of hypoxia, ischemia and inflammation. Both receptor classes are strongly expressed on wound macrophages as well as other cell types. To determine whether the synergistic up-regulation of VEGF expression by TLR and adenosine agonists plays a role in wound healing in vivo, we plan to study wound healing in the skin of mice that lack a critical mediator of the TLR signaling pathway, namely MyD88. MyD88 is the immediate intracellular down-stream mediator of TLR signaling, and has been found in Dr. Leibovich's lab to be absolutely required for the synergistic up-regulation of VEGF expression by TLR agonists with adenosine agonists. The proposed studies in MyD88 knockout mice will illuminate the role of this pathway in vivo in skin wound repair. To this end, we will study various parameters of wound healing in full-thickness excisional skin wounds in MyD88- /- versus MyD88+/+ mice. Establishing the relevance of this synergistic pathway to the healing of wounds will pave the way for approaches to modulate and regulate this pathway using pharmacological agents, which will potentially be of major significance for the clinical modulation of wound healing and fibrosis.