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.
Targeting Neutrophil Extracellular Traps to Improve Extremity Trauma Outcomes
Principal Investigator
Michael Sorkin MD
Michael Sorkin MD
Year
2017
2017
Institution
University of Michigan, Section of Plastic Surgery
University of Michigan, Section of Plastic Surgery
Funding Mechanism
National Endowment for Plastic Surgery Grant
National Endowment for Plastic Surgery Grant
Focus Area
Wounds / Scar, General Reconstructive
Wounds / Scar, General Reconstructive
Abstract
With over 100 million individuals affected annually, musculoskeletal trauma poses a unique challenge to clinicians and patients. Beyond the initial injury, patients with complex trauma are at high risk for pathologic healing and development of heterotopic ossification (HO). HO is the pathologic formation of extra-skeletal bone occurring in 20% of patients with severe musculoskeletal trauma, joint arthroplasty, pressure ulcers and burn injuries leading to substantial patient morbidity including chronic pain, open wounds, reduced joint mobility, and the need for surgical excision. We have previously established a mouse trauma model which has allowed us to study the phases of HO formation and to demonstrate that injury site immobilization reduces inflammation and HO. However, there are currently no clinical guidelines that direct immobilization protocols. Furthermore, the mechanism through which immobilization mitigates inflammation remains unknown. Recently, structural components released by neutrophils, known as neutrophil extracellular traps (NETs), have been implicated as critical elements in driving acute inflammation at the HO site and we have demonstrated that mechanical disruption of NETs during limb movement augments inflammation and promotes HO. Our central hypothesis is that early timed temporary immobilization of the affected injury site will mitigate inflammation through stabilization of NETs. Furthermore, pharmacologic inhibition of NET formation and propagation will reduce inflammation necessary for ectopic bone formation and therefore prophylax against HO. In specific aim 1, we will establish an optimal protocol for timed immobilization of the injury site using our validated Achilles tendon burn/tenotomy model. Furthermore, we will identify how mechanical disruption during limb movement alters NETs and validate a pharmacological inhibitor of primary NETosis (CI-Amidine) to reduce neutrophil and macrophage infiltration at the mobile tendon transection site during early phases after injury. In specific aim 2 we will target toll-like receptor 9 (TLR9), a known immune receptor contributing to NETs mediated inflammation, through pharmacologic inhibition (ODN-2088) or genetic loss (TLR-/-) in order to assess the effect of systemic inhibition of secondary NETosis. Our objective is to demonstrate that these novel interventions can mitigate NET formation and prevent HO thus providing the clinician with a powerful treatment armamentarium.
With over 100 million individuals affected annually, musculoskeletal trauma poses a unique challenge to clinicians and patients. Beyond the initial injury, patients with complex trauma are at high risk for pathologic healing and development of heterotopic ossification (HO). HO is the pathologic formation of extra-skeletal bone occurring in 20% of patients with severe musculoskeletal trauma, joint arthroplasty, pressure ulcers and burn injuries leading to substantial patient morbidity including chronic pain, open wounds, reduced joint mobility, and the need for surgical excision. We have previously established a mouse trauma model which has allowed us to study the phases of HO formation and to demonstrate that injury site immobilization reduces inflammation and HO. However, there are currently no clinical guidelines that direct immobilization protocols. Furthermore, the mechanism through which immobilization mitigates inflammation remains unknown. Recently, structural components released by neutrophils, known as neutrophil extracellular traps (NETs), have been implicated as critical elements in driving acute inflammation at the HO site and we have demonstrated that mechanical disruption of NETs during limb movement augments inflammation and promotes HO. Our central hypothesis is that early timed temporary immobilization of the affected injury site will mitigate inflammation through stabilization of NETs. Furthermore, pharmacologic inhibition of NET formation and propagation will reduce inflammation necessary for ectopic bone formation and therefore prophylax against HO. In specific aim 1, we will establish an optimal protocol for timed immobilization of the injury site using our validated Achilles tendon burn/tenotomy model. Furthermore, we will identify how mechanical disruption during limb movement alters NETs and validate a pharmacological inhibitor of primary NETosis (CI-Amidine) to reduce neutrophil and macrophage infiltration at the mobile tendon transection site during early phases after injury. In specific aim 2 we will target toll-like receptor 9 (TLR9), a known immune receptor contributing to NETs mediated inflammation, through pharmacologic inhibition (ODN-2088) or genetic loss (TLR-/-) in order to assess the effect of systemic inhibition of secondary NETosis. Our objective is to demonstrate that these novel interventions can mitigate NET formation and prevent HO thus providing the clinician with a powerful treatment armamentarium.
Biography
While I was born in St. Petersburg, Russia, my family relocated to Germany where I spent the formative years of my professional education. After developing a keen interest in plastic surgery I decided to pursue a career as an academic surgeon. After graduating from medical school, I was privileged to complete a postdoctoral fellowship under the mentorship of Drs. Gurtner and Longaker at Stanford University where I focused on projects in the fields of regenerative medicine, wound healing and tissue engineering. Through their mentorship I acquired a skill set to independently pursue complex scientific projects. I thereafter completed residency training and microsurgery fellowship at the University of Michigan that allowed me to establish a practice caring for primarily cancer patients. During that time I have remained strongly invested in research and have completed research under Dr. Levi's mentorship and was fortunate to receive funding through the PSF. I have joined the Department of Plastic and Reconstructive Surgery at The Ohio State University as Assistant Professor, where I have established a laboratory focused on identifying pathways to mitigate radiation induced soft tissue fibrosis. I believe that support provided through the PSF would form an integral part in building my academic career.
While I was born in St. Petersburg, Russia, my family relocated to Germany where I spent the formative years of my professional education. After developing a keen interest in plastic surgery I decided to pursue a career as an academic surgeon. After graduating from medical school, I was privileged to complete a postdoctoral fellowship under the mentorship of Drs. Gurtner and Longaker at Stanford University where I focused on projects in the fields of regenerative medicine, wound healing and tissue engineering. Through their mentorship I acquired a skill set to independently pursue complex scientific projects. I thereafter completed residency training and microsurgery fellowship at the University of Michigan that allowed me to establish a practice caring for primarily cancer patients. During that time I have remained strongly invested in research and have completed research under Dr. Levi's mentorship and was fortunate to receive funding through the PSF. I have joined the Department of Plastic and Reconstructive Surgery at The Ohio State University as Assistant Professor, where I have established a laboratory focused on identifying pathways to mitigate radiation induced soft tissue fibrosis. I believe that support provided through the PSF would form an integral part in building my academic career.