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.
The Role of Wnt Signaling and FGFR2 in Craniofacial Anomalies
Alison Snyder-Warwick MD
2007
Washington University
Research Fellowship
Cranio/Maxillofacial/Head and Neck
Previous work in our laboratory has demonstrated reduced FGFR2 signaling in the palate in a mouse model for Crouzon syndrome. Mice with the mutation have high arched or cleft palates. One of the findings associated with this work has been the demonstration of reduced levels of B-catenin (Catnb) in the palate. B-catenin is a key mediator for WNT signaling. Proteins of the Wnt family are secreted factors regulating cell proliferation, fate, and behavior during development, and are required for early craniofacial and tooth development (Kim-Weroha et aI., 2006). Microarray screening of palatal tissue from mice heterozygous for the Crouzon mutation revealed that transcripts for several genes of the Wnt family were decreased. A DermolCre; B-catenin c/c mouse construct available in our laboratory was also analyzed for a cleft palate phenotype. Analysis of these mice at E18.5 revealed cleft palate in 5/5 specimens. The palate of DermolCre; B-catenin c/c mice is much narrower than that of WT mice. It is also steeply angulated and further resembles the Byzantine arch-type palate frequently seen in humans with different types of syndromic craniosynostosis. We hypothesize that loss of Fgfr 2 signaling affects the Wnt signaling pathway and that disruption of Wnt signaling is in part responsible for the associated phenotype. Our specific objective is to characterize Wnt signaling and p-catenin levels and subsequent effects on downstream signaling pathways during palatogenesis and to link these findings to specific developmental anomalies seen in individuals with syndromic craniosynostosis.
