Plastic Surgery Research Council
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PSRC 60th Annual Meeting

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Propranolol Accelerates Involution In A Murine Model Of Infantile Hemangioma
Naikhoba C.O. Munabi, B.A., Ryan W. England, B.S., Kyle J. Glithero, M.D., Michelle M. Chang, B.S., Alex Kitajewski, B.A., Jan K. Kitajewski, Ph.D., Carrie J. Shawber, Ph.D., June K. Wu, M.D..
Columbia University, New York, NY, USA.

PURPOSE:
Propranolol has shown efficacy in the treatment of problematic infantile hemangiomas (IHs). Propranolol achieves this in part via an anti-vasculogenic effect on hemangioma endothelial cells. Previous studies in our laboratory suggested that propranolol induces accelerated adipogenesis of hemangioma stem cells (HemSCs) in culture. The goal of this study is to investigate the effects of propranolol treatment in a murine model of IH. We hypothesize that systemic propranolol will accelerate involution by affecting both vasculogenesis and adipogenesis.
METHODS:
HemSCs isolated from human specimens and suspended in matrigel were injected subcutaneously into immunodeficient mice. Twenty-four hours after injection, mice were continuously administered oral propranolol or vehicle solution. Ultrasound (US) Doppler imaging of matrigel implants was performed weekly to assess for vascular flow. After 3 weeks, the matrigel implants were harvested and H&Es performed. Selected sections were examined for vascular density, vessel diameter, cellularity, total adipose content and number of adipocytes at 20X magnification.
RESULTS:
US doppler of implants detected the presence of blood flow in mice receiving vehicle solution at 2 weeks after implantation (Fig 1). In contrast, there was an absence of discernable flow to the propranolol treated mice at the 3-week endpoint. Histologically, propranolol-treated IHs showed a 33% decrease in vascular density and 50% reduction in vessel caliber when compared to controls (p < 0.0001, Fig 2). Total adipose content was unchanged between vehicle and treatment groups. However adipocyte size was decreased in the propranolol-treated implant resulting in a significant increase in adipocyte number (p < 0.05, Fig 3). Despite the increase in adipocyte number, overall cellularity of the propranolol-treated implant was statistically reduced when compared to control (p < 0.005, Fig 3).
CONCLUSION:
Propranolol treatment led to a loss of detectable blood flow, which correlated with decreased vessel density and caliber in a murine IH model. Propranolol treatment also resulted in increased adipocytes in the setting of decreased cellularity, which are hallmark characteristics of involuting IHs. These findings are consistent with published in vitro data and suggest that propranolol treatment accelerates involution of IH in this murine model.



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