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  • 1
    ISSN: 1432-069X
    Keywords: Key words Graft-versus-host disease ; Murine ; Apoptosis ; Keratinocyte ; Bone marrow transplantation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The skin is a primary target organ in acute graft-versus-host disease (GVHD). Recent results suggest that keratinocytes may undergo apoptosis in acute GVHD, although sequential structural evidence supporting this concept is lacking. The present study was undertaken to document and characterize apoptosis, confirmed by endonuclease-mediated DNA fragmentation, in experimental acute GVHD via sequential analysis of ultrastructure. Furthermore, we sought to define whether apoptosis is effector cell-dependent or -independent, and to document cell types responsible for the scavenging of apoptotic cells. Acute GVHD was produced across minor histocompatibility loci using appropriately matched murine strains and highly purified preparations of donor CD4 + and CD8 + T-cell subsets. Transmission electron microscopy was correlated with in situ labeling of double-stranded DNA breaks by the TUNEL (terminal uridine deoxynucleotidyl transferase end ligation) technique. Apoptotic cells were observed in all groups receiving T cells. Although most apoptotic cells were found in apposition with effector lymphocytes, a minority of apoptotic cells were detected at early time-points prior to lymphocytic infiltration. Heterogeneous cells, including macrophages, lymphocytes, Langerhans cells and keratinocytes were involved in scavenging putative target cells undergoing apoptosis. This study confirms the final pathway of target cell injury in acute GVHD to be apoptosis. In acute GVHD, apoptosis can be induced in the presence or absence of local effector cell influx, suggesting at least two mechanisms for the induction of epidermal target cell injury.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1439-0264
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: This study was undertaken to investigate the immunohistochemical characterization of different subpopulations of macrophages and dendritic cells (DCs) of the spleen, thymus, tongue and heart in cyclophosphamide (CY)-induced immunosuppressed rat. After CY treatment, remarkably, ED1+, ED2+ and ED3+ macrophage subpopulations, in general, exhibited signs of cellular activation such as an increase in number and size of cell, and an upregulation of the ED1, ED2 and ED3 reactive surface molecule expression in all the organs studied, except for some macrophage subpopulations including ED1+ macrophages in the non-lymphoid tissues. Subpopulations of DCs showed a differential sensitivity to CY. Lymphoid DCs were more sensitive to CY than non-lymphoid interstitial DCs. CY induced a conspicuous upregulation of intercellular adhesion molecule-1 (ICAM-1) expression in the vascular endothelial cells, splenic marginal zone and thymic cortex. In this study, we demonstrated the in vivo effects of CY treatment on subpopulations of macrophages and DCs as well as on ICAM-1 expression in the rat spleen, thymus, tongue and heart. Moreover, our results shed more light on the activation effects of CY on certain subpopulations of macrophages, on the differential sensitivity of DCs to CY between the immature and mature ones, on the functional role of different subpopulations of macrophages, and on the significance of upregulated ICAM-1 expression in the splenic marginal zone and thymic cortex after CY treatment.
    Type of Medium: Electronic Resource
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  • 3
    Publication Date: 2018-11-14
    Description: Nonalcoholic fatty liver disease (NAFLD) is an increasingly studied condition that can progress to end-stage liver disease. Although NAFLD was first described in 1980, a complete understanding of the mechanism and causes of this disease is still lacking. Six-transmembrane protein of prostate 2 (STAMP2) plays a role in integrating inflammatory and nutritional signals with metabolism. Our previous study suggested that STAMP2 may be a suitable target for treating NAFLD. In the current study, we performed a focused drug-screening and found that cilostazol could be a potential STAMP2 enhancer. Thus, we examined whether cilostazol alleviates NAFLD through STAMP2. The in vivo and in vitro pharmacological efficacies of cilostazol on STAMP2 expression and lipid accumulation were analyzed in NAFLD mice induced by high-fat diet (HFD) and in HepG2 cell lines treated by oleic acid (OA), respectively. Cilostazol increased the expression of STAMP2 through transcriptional regulation in vivo and in vitro. Cilostazol also dampened the STAMP2 downregulation caused by the HFD and by OA in vivo and in vitro, respectively. Cilostazol activated AMP-activated protein kinase (AMPK) in vivo and in vitro, and AMPK functions upstream of STAMP2, and reversed downregulation of STAMP2 expression through AMPK in the NAFLD model. Cilostazol ameliorates hepatic steatosis by enhancing hepatic STAMP2 expression through AMPK. Enhancing STAMP2 expression with cilostazol represents a potential therapeutic avenue for treatment of NAFLD.
    Print ISSN: 0026-895X
    Electronic ISSN: 1521-0111
    Topics: Chemistry and Pharmacology , Medicine
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