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Oral Inactive Vd3 Enhances Recipient Bed Revascularization and Adipocyte Replacement In Fat Grafts in a Xenograft Model
Alexandra M. Vagonis, BA - University of Pittsburgh, Pittsburgh PA, USA
Shawn J. Loder, MD - University of Pittsburgh, Pittsburgh PA, USA
Bahaa Shaaban, MD, MS, MA - University of Pittsburgh, Pittsburgh PA, USA
Divya Ramkumar, BS - University of Pittsburgh, Pittsburgh PA, USA
Rachel E. Ricketts, BS - University of Pittsburgh, Pittsburgh PA, USA
Wayne V. Nerone, BA - University of Pittsburgh, Pittsburgh PA, USA
Charles Amurgis, BSE - University of Pittsburgh, Pittsburgh PA, USA
Phoebe Lee, BS - University of Pittsburgh, Pittsburgh PA, USA
J. Peter Rubin, MD, MBA, FACS - University of Pittsburgh, Pittsburgh PA, USA
Lauren E. Kokai, PhD - University of Pittsburgh, Pittsburgh PA, USA
University of Pittsburgh Department of Plastic Surgery
2023-02-01
Presenter: Alexandra Vagonis
Affidavit:
I certify that the material proposed for presentation in this abstract has not been published in any scientific journal or previously presented at a major meeting. While this presentation involves a new findings from a portion of a larger ongoing project within our lab, I verify that the research fellow has performed and analyzed a substantial portion of the work included in this presentation.
Director Name: Lauren E. Kokai
Author Category: Medical Student
Presentation Category: Basic Science Research
Abstract Category: General Reconstruction
PURPOSE: Fat grafting is limited by unpredictable retention. We previously demonstrated that bioactive VD3 improves human fat graft retention in a xenograft mouse model; however, high doses incur safety risks. We have also shown that oral, inactive VD3 is equally effective at increasing graft retention, without the associated risks, and enhances endothelial cell proliferation, migration, and invasion with in vivo models. Increased recipient bed revascularization and adipocyte replacement may support this improvement in graft retention. Our study aims to confirm the origin of vasculature responsible for xenograft revascularization and adipocyte repopulation.
METHODS: Mouse-CD31 chromogenic IHC staining was performed on mouse tissue containing xenografted human fat, that had been treated with 50, 500, or 5000 IU of inactive VD3 or received none. Human-CD31 chromogenic IHC staining was performed on xenografted human, control mouse, and control human fat. Human-specific perilipin 4 (PLIN4) IF staining was performed on xenografted human fat, control mouse, and control human fat.
RESULTS: Mouse-CD31 showed increased intra-graft staining of mouse-derived endothelial cells present throughout those treated with 50, 500, and 5000 IU VD3, compared to untreated grafts. Human-CD31 demonstrated pan-reactivity with both human and mouse intra-graft endothelial cells. Human-PLIN4 showed intense yet non-uniform fluorescence within the xenografted adipose, intense staining throughout human control adipose, and minimally staining control mouse adipose.
CONCLUSIONS: The abundance of intra-graft mouse-derived endothelial cells suggests that revascularization is recipient-driven and appears to be VD3 dose-dependent. The non-uniform stain intensity of PLIN4 in xenografted adipose suggests mouse-driven adipocyte replacement within the intensely fluorescent human-derived graft.
