The Plastic Surgery Foundation
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Grants We Funded

Grant applicants for the 2023 cycle requested a total of nearly $4 million dollars. The PSF Study Section Subcommittees of Basic & Translational Research and Clinical Research evaluated nearly 140 grant applications on the following topics:

The PSF awarded research grants totaling over $1 million dollars to support nearly 30 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.

Investigating the Role of Myofibroblasts in Wound Healing

Principal Investigator
Mark Fisher MD

Year
2011

Institution
Duke University

Funding Mechanism


Focus Area


Abstract
The incidence of contracture formation in burns is ~ 40%. There are no effective treatments to prevent contractures. Contractures continuously shrink over time as a result of cell contractility. Cell contractility is caused by actomyosin force generation. There are three forms of actin: ß-cytoplasmic (ß-actin), ?-cytoplasmic (?-actin), and a-smooth muscle actin (a-SMA). aSMA is the characteristic form of actin present in contractile myofibroblasts. But the three actin isoforms may substitute for each other to cause contracture formation. We will test the hypothesis that ß-actin and ?-actin can substitute for aSMA to promote scar contracture and fibroblast contractility. The long-term objective is to develop a drug to prevent and treat contracture formation. Specific Aim 1 To characterize the specific role of aSMA within the inflammatory, proliferative, and remodeling phases of repair that cause scarring in vivo. Wound models representative of all phases of wound healing will be performed in wild-type, aSMA KO, and heterozygous mice for aSMA. The wounds will be comprehensively analyzed using methods aimed at the unique charactistics of each phase. These will include gross appearance, rate of contraction, histology, and immunohistochemistry. qRT-PCR will be used to quantify the actin isoforms. And wound breaking strength will also be used to assess the remodeling phase. Specific Aim 2. To determine how a-sma, ß-actin, and ?-actin expression alter fibroblast contractility. This Specific Aim will transfect a-sma KO fibroblasts with ß-actin and ?-actin siRNA to determine whether ß-actin, and ?-actin can substitute for a-sma to produce the same contractile forces. Contractile forces will be measured using fibroblast populated collagen lattice contraction, and fibroblast migration assays.