Grants Funded
Grant applicants for the 2024 cycle requested a total of nearly $3 million dollars. The PSF Study Section Subcommittees of Basic & Translational Research and Clinical Research evaluated more than 100 grant applications on the following topics:
The PSF awarded research grants totaling over $650,000 dollars to support more than 20 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.
Mechanotransduction in Adverse Implant-Tissue Interactions
Jagannath Padmanabhan MD
2018
Stanford University
PSRC/ PSF Research Grant
Wounds / Scar, General Reconstructive
Biomedical implant performance and longevity is primarily limited by foreign body reaction (FBR), which is a fibrotic reaction characterized by accumulation of cells, proteins, and other biological materials on the implant surface. Varying degrees of FBR towards biomedical implants has been well documented. Severe FBR leads to formation of thick collagen-rich encapsulations (FBR capsules), poor implant-tissue integration and implant rejection. We have previously shown that severe fibrosis during wound healing, a process closely related to FBR, is mediated by mechanical force in a process termed mechanotransduction. The role of mechanotransduction in FBR is not clear. In particular, which specific cells (i.e. transcriptionally activated subpopulations of macrophages, fibroblasts etc.) are involved in severe FBR and how mechanical cues activate these cells remains unknown. Our preliminary work has developed a novel animal model to study severe FBR, identified a mechanotransduction pathway that could mediate severe FBR and established a strategy to identify transcriptionally distinct cells in FBR capsules. Specifically, I have developed a prototype animal model termed “hyper FBR”. Briefly, mechanical vibration of model silicone implants in mice using a coin motor results in increased fibrotic response (hyper FBR) as compared to non-vibrating control implants. I have also analyzed human FBR capsules using mass spectrometry, which revealed that that the PI3-Akt pathway is upregulated in FBR capsules. PI3-Akt pathway has been previously implicated in fibrotic wound healing. Further, our lab has developed a strategy combining single cell transcriptional analyses with surface marker screening to identify transcriptionally distinct cell subpopulations, which can be employed to interrogate cells that mediate FBR. My central hypothesis is that activation of cells expressing the PI3-Akt mechanotransduction pathway leads to adverse implant-tissue interactions. I propose to define key mechanoresponsive cells in human FBR capsules and the hyper FBR animal model. Specifically, single cells isolated from FBR capsules will be analyzed for the expression of PI3-Akt and related mechanotransduction pathway components to identify cells with high PI3-Akt expression that can be used as targets to limit FBR. Finally, we will test the efficacy of using inhibitors against the PI3-Akt pathway to limit FBR.
