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.
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.
Hemangiomas: Stem Cell Tumors of Pericyte Origin
Deepak Narayan MD
Yale University School of Medicine
Pilot Research Grant
Cranio / Maxillofacial / Head and Neck, Other
Hemangiomas are the most common tumors of infancy predominantly affecting the head and neck. They are vascular tumor comprised of endothelial cells. However, little is known about their origin. Nearly all lesions turn into a fibrofatty residuum, suggesting a default pathway that converts them into fat. We wish to propose a novel hypothesis that hemangiomas are stem cell tumors comprised of pericytes derived from the neural crest. Based on this premise we will investigate a novel drug treatment that forces hemangiomas into the default adipocyte pathway. In an animal model, pericytes were precursors to adipocytes.(Tang et al. 2008) We hypothesize that markers for pericytes will be present in hemangioma tissue. Delta like kinase(dlk) is a critical inhibitory factor that controls the maturation of preadipocytes to adipocytes and is a strong marker of pericytes. To show the link between pericytes and hemangiomas, we will infect hemangioma cultures with a dlk silencing gene with the hypothesis that silencing dlk will cause the hemangioma to turn to fat. We will also analyze microRNAs that regulate adipocyte formation, mi195, mi299 and mi143. Dupin et al. have shown that pericytes as well as a significant component of the soft tissue of the head and neck region are derived from the neural crest. We hypothesize that hemangioma tissue will demonstrate neural crest markers accounting for its predilection to the head and neck region as well as stem cell markers given these cells' phenotypic malleabilty. In order to demonstrate the presence of pericyte, neural crest, and stem cell markers we will selectively excise tissue with laser capture microdissection followed by RNA extraction and qRTPCR for selected markers.
Finally, hemangioma tissue will be placed subcutaneously in mice and treated with thiazolidionediene(TZD). TZD acts on dlk and PPARgamma, both involved in adipogenesis.
This will add to the understanding of pathogenesis and treatment of hemangiomas.