Abstract
Infantile hemangioma is a common tumor of infancy. Although most hemangiomas spontaneously regress, treatment is indicated based on complications, risk to organ development and function, and disfigurement. The serendipitous discovery of propranolol, a non-selective β-adrenergic receptor blocker, as an effective means to regress hemangiomas has made this a first-line therapy for hemangioma patients. Propranolol has shown remarkable response rates. There are, however, some adverse effects, which include changes in sleep, acrocyanosis, hypotension, and hypoglycemia. Over the last few years, researchers have focused on understanding the mechanisms by which propranolol causes hemangioma regression. This has entailed study of cultured vascular endothelial cells including endothelial cells isolated from hemangioma patients. In this article, we review recent studies offering potential mechanisms of how various cell types found in hemangioma may respond to propranolol.
Highlights
It has been shown that hemangioma-derived endothelial cells (hemECs) and other endothelial cell (EC) types express both b1- and b2-adrenergic receptor (ADR) at very similar levels, but not b3.52,53 We have shown that normal ECs express all 3 b-adrenergic receptors (b-ADRs), with b1-ADR expression being significantly higher when compared to the other subtypes.[50]
Continuous culture of hemangioma stem cells (hemSCs) in adipogenic differentiation media supplemented with propranolol causes cell death.[31]. These results suggested that propranolol treatment accelerated the dysregulated differentiation process in hemSCs that resulted in increased apoptosis of adipocytes derived from hemSCs.[31]
Dermato-Endocrinology studies have suggested that the use of b-blockers is effective in treating several tumors and cancers. b-ADR subtypes are associated with cancer growth and progression by increasing angiogenic, migratory, and invasive factors in tumor cells
Summary
Over the last few years, researchers have focused on understanding the mechanisms by which propranolol causes hemangioma regression. This has entailed study of cultured vascular endothelial cells including endothelial cells isolated from hemangioma patients. An example of such a situation is the growth of IH in the airway to obstruct the respiratory system.[16]
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