The goal of this Core is to provide hemangioma-derived cells and hemangioma tissue for analyses related to each of the three projects in this program project grant. Cells are purified, characterized by immunophenotyping, RT-PCR, and morphological analyses. The cells are cryopreserved in liquid nitrogen, and tracked by an Excel based inventory system. Over 100 hemangioma tissues from proliferating, involuting and involuted phases is available for RNA, DNA and tissue analyses. This represents an invaluable resource of studies on cellular and molecular mechanisms that cause infantile hemangioma. The Core will continue to add new primary cultures of hemangioma-derived cells, normal human microvascular EC and hemangioma tissues to this cell and tissue bank so that the spectrum of hemangioma samples is continuously replenished and available to all investigators working on this PPG. A specific focus of Core B in the requested funding period will be to fully characterize hemangioma-derived stem cells for use by investigators on this PPG. Training and technical support for endothelial cell isolation, expansion, and characterization will be available to the investigators on this PPG through the website, phone/e-mail communication, and hands-on training when required. In summary, this Core is an essential resource for the success of the Program Project.
Core B will provide carefully characterized cell populations isolated from hemangioma tissue obtained when a hemangioma tumor is removed from a child as part of his/her clinical care. The tissue and the isolated cells provide powerful tools for the study of what causes the abnormal growth in hemangioma and also important tools for testing new treatments to prevent hemangioma formation and/or to accelerate involution.
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|Lee, D; Boscolo, E; Durham, J T et al. (2014) Propranolol targets the contractility of infantile haemangioma-derived pericytes. Br J Dermatol 171:1129-37|
|Dellinger, Michael T; Garg, Nupur; Olsen, Bjorn R (2014) Viewpoints on vessels and vanishing bones in Gorham-Stout disease. Bone 63:47-52|
|Uebelhoer, Melanie; Natynki, Marjut; Kangas, Jaakko et al. (2013) Venous malformation-causative TIE2 mutations mediate an AKT-dependent decrease in PDGFB. Hum Mol Genet 22:3438-48|
|Amyere, Mustapha; Aerts, Virginie; Brouillard, Pascal et al. (2013) Somatic uniparental isodisomy explains multifocality of glomuvenous malformations. Am J Hum Genet 92:188-96|
|Butler, Matthew G; Dagenais, Susan L; Garcia-Perez, Jose L et al. (2012) Microcephaly, intellectual impairment, bilateral vesicoureteral reflux, distichiasis, and glomuvenous malformations associated with a 16q24.3 contiguous gene deletion and a Glomulin mutation. Am J Med Genet A 158A:839-49|
|Greenberger, Shoshana; Yuan, Siming; Walsh, Logan A et al. (2011) Rapamycin suppresses self-renewal and vasculogenic potential of stem cells isolated from infantile hemangioma. J Invest Dermatol 131:2467-76|
|Goujon, Elisa; Cordoro, Kelly M; Barat, Muriel et al. (2011) Congenital plaque-type glomuvenous malformations associated with fetal pleural effusion and ascites. Pediatr Dermatol 28:528-31|
|Boon, Laurence M; Ballieux, Fanny; Vikkula, Miikka (2011) Pathogenesis of vascular anomalies. Clin Plast Surg 38:7-19|
|Bowen, Margot E; Boyden, Eric D; Holm, Ingrid A et al. (2011) Loss-of-function mutations in PTPN11 cause metachondromatosis, but not Ollier disease or Maffucci syndrome. PLoS Genet 7:e1002050|
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