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Articles by Carl G. Figdor
Total Records ( 2 ) for Carl G. Figdor
  Bellinda A. Bladergroen , Els den Dekker , Kim G.C. Vermeulen , Tanja Netelenbos , Angelika M. Drager , Konnie M. Hebeda , Carl G. Figdor and Ruurd Torensma
  In bone marrow niches, direct interactions of Hematopoetic Stem Cells (HSCs) with supportive stromal cells and the extracellular matrix are essential for regulation of hematopoiesis. These interactions are mediated by several sets of adhesion molecules. In vivo, different adhesion molecules were spatially separated and showed specific distributions for the different adhesion molecules. These patterns for VLA-2, VLA-3, ALCAM, VLA-1, VLA-4, VCAM-1 and ICAM-3, varied in size, ranging from a single cell to smaller or larger cell clusters. ICAM-1 and VLA-5 were expressed by virtually all cells. The results are similar in seven individual steady state bone marrows. In vitro, adhesion molecule expression changed for several stromal cell types by exposing them to different inductors as present in different animal sera. Besides the normal blood cell turn over recruitment of more blood cell developmental centers is needed during increased demands for hematopoietic cells. During infection far more granulocytes are demanded by the organism than during normal turnover. Such adaptation to changing conditions is easily accomplished by highly flexible spatio-temporal distribution of adhesion molecules since it provides bone marrow stromal cells with the capacity to deliver the specific lineages that the organism demands.
  R. Torensma , Rene H.J. Brouwer , Karin Van Ginkel , Carl G. Figdor and Sandeep K. Singh
  This study was designed to unravel if arterial grafts treated with phosphate buffered saline or 10Gy irradiation to induce endothelial cell loss, still contain enough biological information to drive proper endothelial regeneration. To demonstrate that damage to donor arteries retains the biological information needed to drive proper differentiation of circulating endothelial precursor cells, arteries were either irradiated (n=10) (10Gy) or stored for 30 min in PBS (n=10) at 20 C. After treatment the arteries were grafted end to end in the aorta descendens of GFP transgenic rats. Three weeks after implantation 5 grafts were recovered and the remaining 5 after 6 weeks and were analyzed immuno histochemically using antibodies to endothelial cell lineage markers (CD31 and von Willebrand factor), Griffiona simplicifolia lectin and Green Fluorescent Protein (GFP). Arteries processed immediately after surgery served as control. Grafted arteries had an intact endothelial layer. Three weeks after graft implantation the arteries were totally denuded for both treatment protocols, while cells attach to the fibroelastic layer. Six weeks after grafting the grafts showed neointima formation and were totally reendothelialized with recipient cells. The fibroelastic layer and adventitia also contained green recipient cells. These results provide compelling evidence that mild treated arteries loose their endothelial lining but still contain the biological information to drive endothelial differentiation of recipient circulating endothelial precursor cells resulting in a intact endothelial layer six weeks after surgery. This in contrast to harsh treated grafts.
 
 
 
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