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.
Elucidating the Intracellular Signaling Events Responsible for Strain-Dependent Bone Formation
Pierre Saadeh MD
2006
New York University Medical Center
Basic Research Grant
Cranio/Maxillofacial/Head and Neck
Mechanical forces can affect cellular behavior. Distraction osteogenesis (DO) applies mechanical force to cells in the distraction gap, stimulating new bone formation. In vivo experiments demonstrate that in the bone generate, a collagen framework is constructed, new blood supply is recruited and then the framework is ossified. Building and then ossifying the collagen framework is a delicate balance of complex interactions (e.g. mechanobiology, cell recruitment, cytokine production). Perturbations of this complex system can lead to fibrous union. Alternatively, external manipulation of this system could improve bone formation and shorten therapy. While there are many factors to investigate, elucidating the mechanism of matrix formation (e.g. collagen type I secretion) and ossification (e.g. alkaline phosphatase) in response to tensile strain is essential to improving our understanding of this valuable technique. Evidence suggests that the intracellular signaling molecules: mitogen activated protein kinase (MAPK), phosphoinostitol-3 kinase (PI3K), and the 90 kDa ribosomal S6 kinases (p90RSK), can translate a mechanical stimulus into a cellular response in osteoblasts. However, there is a paucity of data linking strain-induced activation of intracellular pathways to bone formation. The central hypothesis of this proposal is that strain-dependent collagen I and alkaline phosphatase gene expression are regulated by the MAPK and PI3K pathways in osteoblasts.