What is it about?
Angiogenesis inhibition is vital to treat hemangioma. Propranolol (PRO) inhibition of angiogenesis may play a key role in the accelerated hemangioma involution, but the mechanisms underlying are unclear. hemangioma-derived endothelial cells (HemECs) were cultured in vitro, and a BALB/c nude mice hemangioma model was established. Viability and proliferation of HemECs, and the role of thrombospondin-1 and nuclear factor-kappa B signaling pathways were observed after PRO administration in vitro and in vivo. This study described a new mechanism of tumor angiogenesis and regression in hemangioma, and provided a new target for hemangioma treatment.
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Why is it important?
We analyzed hemangioma-derived endothelial cells viability and proliferation, and the role of thrombospondin-1 and nuclear factor-kappa B signaling pathways after administration of propranolol. Our results showed a new mechanism of tumor angiogenesis and regression in hemangioma associated with thrombospondin-1 and nuclear factor-kappa B, and provided new targets for hemangioma treatment. We believe that our study makes a significant contribution to the literature because new effective therapeutic methods for the treatment of diseases such as hemangioma are necessary.
Perspectives
The present study provided the new targets for the clinical treatment of infantile hemangioma. Writing this article was a great pleasure as it has co-authors with whom I have had long standing collaborations. This article also lead to hemangioma groups contacting me and ultimately to a greater involvement in hemangioma research.
Weili XU
The Second Hospital of Hebei Medical University, China
Read the Original
This page is a summary of: Role of thrombospondin-1 and nuclear factor-kappa B signaling pathways in anti-angiogenesis of infantile hemangioma, Plastic & Reconstructive Surgery, June 2018, Wolters Kluwer Health,
DOI: 10.1097/prs.0000000000004684.
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