Follicular dendritic cell tumor of the mediastinum: expression of fractalkine and SDF-1alpha as mast cell chemoattractants.

Follicular dendritic cell tumor (FDCT) is a rare tumor mainly located in laterocervical lymph nodes. We report one case of mediastinal FDCT associated with a history of bullous skin disease and clinically obvious immunosuppression. This tumor was characterized by heavy mast cell infiltration. Mast cells were in close relationship with tumor cells as demonstrated by ultrastructural examination and their presence are probably related with the strong expression of mast cell chemoattractants as fraktalkine and stromal cell-derived factor-1alpha by tumor cells. The long follow-up period of more than 17 years allowed to us assess the relatively indolent evolution of this tumor characterized by three slowly growing local recurrences without metastasis.

Human endothelial cells derived from circulating progenitors display specific functional properties compared with mature vessel wall endothelial cells.

Endothelial progenitor cells (EPCs) were shown to be present in systemic circulation and cord blood. We investigated whether EPCs display specific properties compared with mature endothelial cells. Human cord blood CD34+ cells were isolated and adherent cells were amplified under endothelial conditions. Expression of specific markers identified them as endothelial cells, also called endothelial progenitor-derived cells (EPDCs). When compared to mature endothelial cells, human umbilical vein endothelial cells (HUVECs) and human bone marrow endothelial cells (HBMECs), endothelial markers, were expressed to the same extent except for KDR, which is expressed more in EPDCs. They display a higher proliferation potential. Functional studies demonstrated that EPDCs were more sensitive to angiogenic factors, which afford these cells greater protection against cell death compared with HUVECs. Moreover, EPDCs exhibit more hematopoietic supportive activity than HUVECs. Finally, studies in nonobese diabetic/severe combined immunodeficiency (NOD/SCID) mice demonstrated that human circulating EPCs are able to colonize a Matrigel plug. EPDCs display the morphology and phenotype of endothelial cells. Their functional features indicate, however, that although these cells have undergone some differentiation steps, they still have the properties of immature cells, suggesting greater tissue repair capabilities. Future use of in vitro amplified peripheral blood EPDCs may constitute a challenging strategy for cell therapy.

Beneficial effect of pentoxifylline on microvesicular steatotic livers submitted to a prolonged cold ischemia.

BACKGROUND: The deleterious effect of steatosis on transplanted livers is mainly related to a microcirculation impairment. We investigated the effect of preservation duration on the recovery of isolated perfused rat steatotic livers and tested the effect of pentoxifylline (PTX), known to have a beneficial effect on hepatic microcirculation. MATERIALS AND METHODS: Fatty rat livers were obtained using a diet able to induce an 80% to 100% microvesicular steatosis within 7 days. We studied the effect of the duration of preservation (12 hr, 18 hr, and 24 hr) on fatty and normal isolated perfused rat liver. PTX was added to University of Wisconsin solution during cold storage (30 mM/kg of weight) and at reperfusion (3 mM) (n=5 livers in each group). Lactate dehydrogenase, aspartate aminotransferase, alanine aminotransferase, bile production, and vascular resistance were evaluated. The liver injury at the end of perfusion was assessed by optical and electron microscopy. RESULTS: For a 24-hr preservation period, fatty livers demonstrated increased enzymatic release (aspartate aminotransferase: 42+/-16 vs. 17+/-5 IU/L/g of liver, P<0.005; alanine aminotransferase: 32+/-13 vs. 13+/-3 IU/L/g of liver, P<0.005; lactate dehydrogenase: 1,207+/-497 vs. 291+/-195 IU/L/g of liver, P<0.001). Vascular resistance (0.32 vs. 0.15 cm H(2)O/min/mL, P<0.0005) and bile output (67+/-24 vs. 141+/-61 mg/g of liver, P<0.05) were decreased. Peliosis appeared after an 18-hr preservation period for fatty livers compared with a 24-hr preservation period for controls. All these negative effects were suppressed by PTX. CONCLUSION: Diffuse microvesicular steatosis became deleterious only after long preservation times (24 hr). PTX prevented this effect.

Fetal liver stroma consists of cells in epithelial-to-mesenchymal transition.

Liver becomes the predominant site of hematopoiesis by 11.5 dpc (days after coitus) in the mouse and 15 gestational weeks in humans and stays so until the end of gestation. The reason the liver is the major hematopoietic site during fetal life is not clear. In this work, we tried to define which of the fetal liver microenvironmental cell populations would be associated with the development of hematopoiesis and found that a population of cells with mixed endodermal and mesodermal features corresponded to hematopoietic-supportive fetal liver stroma. Stromal cells generated from primary cultures or stromal lines from mouse or human fetal liver in the hematopoietic florid phase expressed both mesenchymal markers (vimentin, osteopontin, collagen I, alpha smooth muscle actin, thrombospondin-1, EDa fibronectin, calponin, Stro-1 antigens, myocyte-enhancer factor 2C) and epithelial (alpha-fetoprotein, cytokeratins 8 and 18, albumin, E-cadherin, hepatocyte nuclear factor 3 alpha) markers. Such a cell population fits with the description of cells in epithelial-to-mesenchymal transition (EMT), often observed during development, including that of the liver. The hematopoietic supportive capacity of EMT cells was lost after hepatocytic maturation, induced by oncostatin M in the cell line AFT024. EMT cells were observed in the fetal liver microenvironment during the hematopoietic phase but not in nonhematopoietic liver by the end of gestation and in the adult. EMT cells represent a novel stromal cell type that may be generated from hepatic endodermal or mesenchymal stem cells or even from circulating hematopoietic stem cells (HSCs) seeding the liver rudiment.