Background: Infantile hemangioma (IH) is the most frequent vascular tumor of early childhood. Recently, propranolol, a nonselective β1- and β2-adrenoceptor inhibitor, was introduced into the therapy of severe proliferating IH with excellent results. However, the underlying mechanism of action of propranolol is still unclear.
Methods: We performed immunohistochemistry for cluster of differentiation 31 (CD31), D2-40, glucose transporter-1 (GLUT-1), and Ki67 in order to characterize 21 vascular anomalies (nine IH, seven venous malformations (VMs), and five lymphatic malformations (LMs)). Furthermore, we analyzed the expression of β1-, β2-, and β3-adrenoceptor mRNA in these specimens as well as in hemangioma-derived stem cells by quantitative real-time PCR (qPCR).
Results: We show that the expression of β1-adrenoceptor mRNA is 10.7-fold higher in IH independent of the proliferative or regressive phase as well as 2.5-fold higher in hemangioma-derived stem cells as compared with β2-adrenoceptor mRNA. In LM, the expression of β2-adrenoceptor mRNA was ninefold higher than that of β1-adrenoceptor mRNA. VM showed low expression levels of all β-adrenoceptor mRNAs, and β3-adrenoceptor mRNA was hardly detectable in any specimens examined.
Conclusion: These results provide the first evidence of distinctions between IH and vascular malformations with regard to β-adrenoceptor subtype mRNA levels.