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.
Contribution of Merlin Inactivation in Facial Nerve Schwann Cell Regeneration
Richard Gurgel MD
University of Iowa
PSF/AAO-HHNF Academic Scholar Research Grant
Regeneration of facial nerve axons following injury critically depends on support provided by the Schwann cells (SCs). Following nerve injury, SCs dedifferentiate, proliferate, and provide support for eventual axonal regrowth. The molecular mechanisms regulating the response of SCs to loss of axonal contact are unclear. Merlin is the product of the nf2 tumor suppressor gene which mediates SC-axon contact information to regulate cell proliferation and survival. Phosphorylation of serine 518 (S518) inactivates the growth suppressive function of merlin, facilitating proliferation. Protein kinase A (PKA) phosphorylates merlin S518 during SC proliferation. We hypothesize that denervation results in merlin inactivation by phosphorylation of serine 518 (S518) by protein kinase A (PKA) and that this is necessary for SC proliferation. Aim 1: Determine whether PKA activity is required in vivo for merlin S518 phosphorylation and FN SC proliferation following axotomy. In preliminary studies, we show that merlin becomes phosphorylated on S518 following axotomy and that this correlates with SC proliferation. We will test the requirement of PKA activity in mediating these responses. Following facial nerve axotomy, rats will be treated with KT5720, a specific PKA, inhibitor delivered via a minipump. Merlin phosphorylation will be assessed by Western blot and immunofluorescence to quantify the SC proliferation in treated vs. control nerves in vivo. Aim 2: Determine if merlin S518 phosphorylation by PKA is necessary for SC proliferation. In preliminary studies, we show that activation of PKA with forskolin (FSK) results in merlin S518 phosphorylation and increases SC proliferation. To establish a causative relationship between PKA-induced merlin S518 phosphorylation and SC proliferation, we will use adenovirus-mediated gene transfer to introduce wild-type or S518-mutated merlin isoforms into primary schwannomas cells which lack merlin. S518A mutations render merlin unable to be phosphorylated while S518D mutations are phosphomimetic. We will compare the percent of proliferating cells expressing the merlin isoforms in the different conditions. Facial nerve regeneration following injury depends on support by SCs. Understanding the molecular events that regulate the response of SCs to injury may lead to novel methods to enhance regeneration. Using in vivo and in vitro models, we endeavor to define the requirement of merlin phosphorylation by PKA in promoting facial nerve SC proliferation following loss of axonal contact.