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.
Single Cell Analysis of SDF-1 Mediated Stem Cell Recruitment
Zeshaan Maan MD
Chronic wounds affect more than 6 million Americans, generating an annual healthcare cost of $25 billion. Typically manifesting in elderly and diabetic patients, chronic wounds are related to impaired new blood vessel growth (neovascularization). Developing therapeutics to improve wound healing, therefore, requires intimate knowledge of the mechanism underlying neovascularization. Despite numerous studies demonstrating the importance of stem/progenitor cell recruitment during neovascularization, therapeutic approaches remain limited by an insufficient understanding of the cell populations involved.
Stromal-cell derived factor-1 (SDF-1) has attracted attention as a pivotal regulator of stem/progenitor cell recruitment to sites of ischemia and recent studies have demonstrated a deficiency of SDF-1 in aging and diabetes. At present, the specific stem/progenitor cell population recruited by SDF-1 remains unknown. The Gurtner Lab has developed novel SDF-1 genetic knockout mice to study this. Initial studies have demonstrated a phenotype of poor neovascularization in both global and endothelial knockout mice. Moreover, parabiosis models have demonstrated reduced recruitment of stem/progenitor cells to wounds in the absence of endothelial cell production of SDF-1.
I aim to: 1) assess the SDF-1 mediated recruitment of stem/progenitor cells to sites of ischemia and 2) detect circulating stem/progenitor cell populations recruited by SDF-1 and develop characteristic surface marker profiles using microfluidic-based single cell transcriptional analysis (mSTA). mSTA allows clustering of individual cells into subpopulations, with the bioinformatics expertise in our laboratory facilitating this interdisciplinary approach. The proposed utilization of a novel transgenic mouse model in conjunction with high-throughput gene expression analysis to characterize SDF-1 mediated stem/progenitor cell recruitment will be the first of its kind, providing important insight for the development of future therapies.
Dr. Zeshaan Maan is a postdoctoral research fellow in the Hagey Laboratory for Pediatric Regenerative Medicine at Stanford University School of Medicine under the mentorship of Dr. Geoffrey Gurtner. He moved to the UK after graduating from Bellarmine College Preparatory in San Jose, California and received his medical degree from King’s College London School of Medicine. During his Core Surgical Training, which he completed at St Andrews Centre for Plastic Surgery & Burns (Chelmsford, Essex), he also gained a master’s degree in Surgical Technology from Imperial College London and was inducted as a Member of the Royal College of Surgeons. Since joining the Gurtner Laboratory, Dr. Maan has been investigating cellular and molecular mechanisms of mammalian regeneration, including the role of stem and progenitor cells and the discrete signalling mechanisms governing their function. As a recipient of the 2014-2015 Plastic Surgery Foundation Research Fellowship award, Dr. Maan will focus on understanding the progenitor cell response to ischemia.