The Plastic Surgery Foundation
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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.

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 Effects of Inflammatory Mediators on Capsular Contracture in the Mouse Model

Principal Investigator
Howard Langstein MD


University of Rochester

Funding Mechanism
Pilot Research Grant

Focus Area
Breast (Cosmetic / Reconstructive)

This study's goal is to introduce a new murine model in order to facilitate research into the cellular and molecular pathways underlying capsular. The specific aims of this study are:

Aim 1: To characterize the temporal differences in capsular formation and contracture between irradiated and non-irradiated wildtype mice using uCT, realtime RT-PCR, and histology.

Rationale: The mouse is the only animal in which knockout and transgenic strains can be developed for molecular research. Currently, there is no published mouse model for the study of capsular contracture. We will develop a novel mouse model using livescan uCT, realtime RT-PCR, and histology to study and evaluate capsular contracture.

Aim 2: To characterize the difference in severity of capsular contracture between irradiated and non-irradiated wildtype and Smad3-/- mice using realtime RT-PCR, uCT, and histology.

Rationale: TGF-ß has been linked with both scar formation and radiation injury, and Smad3 plays a critical role in TGF-ß activation. We will elucidate the role of TGF-ß and Smad3 signaling in capsular contracture.
To test this, wildtype and Smad3-/- mice will be implanted with bilateral silicone gel implants (Mentor, Inc.) and receive slit beam radiation. The targeted radiation is designed to induce contracture and prevent systemic effects of radiation. Implant shape and orientation will be evaluated using µCT, gene expression will be quantified using realtime RT-PCR and capsule quality will be evaluated with histology.

This study will develop a murine silicone implant model and test the hypothesis: Smad3 loss of function in the Smad3-/- mouse attenuates the TGF-ß signaling pathway leading to reduced capsular contracture following silicone implant insertion and radiation therapy. This work will provide a model to further study molecular pathways involved in capsular contracture and will translate to molecular based therapies to reduce capsular contracture.

Howard N. Langstein, MD FACS is Professor and Chief of the Division of Plastic Surgery at the University of Rochester School of Medicine, where he specializes in all aspects of breast reconstruction. He trained at New York University in General and Plastic Surgery, at the National Institutes of Health in Surgical Oncology, and at M. D. Anderson Cancer Center in microvascular oncologic reconstruction. He has a research interest in modulating the scar mechanism, particularly the process of capsular contracture around breast implants.