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Increased apoptosis and secretion of tryptase by mast cells in infantile haemangioma treated with propranolol.
MedLine Citation:
PMID:  25158819     Owner:  NLM     Status:  Publisher    
Propranolol is increasingly used to treat problematic infantile haemangioma (IH), although its molecular mechanisms remain unclear. A key feature of propranolol therapy is the decreased deposition of fibrofatty residuum compared with spontaneously involuting IH. This study investigated the molecular consequences of propranolol treatment for IH in vivo. Immunohistochemical and terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL) staining was performed on five age matched patients with proliferative IH. Two patients (A and B) were undergoing propranolol treatment at the time of surgical resection. Propranolol treatment increased apoptosis, and induced mast cells to degranulate and secrete tryptase into the interstitium. The microvessels of patient A were immature [weak von Willibrand Factor (vWF), and strong osteoprotegerin (OPG) staining], comparable to untreated proliferative IH, while those of patient B were mature (strong vWF staining, and no OPG staining). The perivascular CD90 mesenchymal stem cell population was preserved in both propranolol treated patients. Using rarely obtained biopsies from IH patients treated with propranolol, we show increased apoptosis by propranolol for the first time in vivo. We also suggest that mast cells, through secreted proteases, may contribute to the decreased fibrofatty residuum seen with propranolol treatment.
Ryan Steel; Darren Day
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2014-8-25
Journal Detail:
Title:  Pathology     Volume:  -     ISSN:  1465-3931     ISO Abbreviation:  Pathology     Publication Date:  2014 Aug 
Date Detail:
Created Date:  2014-8-27     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0175411     Medline TA:  Pathology     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
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