Endothelial cells donors

Lompre Normally endothelial cells have SERCA2B and SERCA3. Liu et al (1997) showed that SERCA3-defective mice have the same defect in relaxation that you describe. If they add NO donors, they also restore relaxation as for TRP4. Could it be that there is a relationship between this pool of Ca2+ SERCA3 and TRP4 ... 

DETA/NO is a stable NO-donor with the longest NO generation half-life of approximately 20 h. Thrombelastography performed on rabbit blood showed that DETA NONOate-derived NO significantly decreased coagulation activity and platelet activation [48]. Monitoring by intravital microscopy showed that DETA/NO attenuated the platelets/endothelial cells adhesion response to endotoxins (e.g. lipopolysaccharides) in murine intestinal venules [49]. The main mechanism of the antiadhesive action of DETA/NO on platelets was activation of soluble guanylate cyclase [49]. 

The above examples point out at the direct stimulation of apoptosis by nitric oxide. At the same time, the exclusively rapid reaction of NO with superoxide always suggests the possibility of peroxynitrite participation in this process [141] correspondingly, the role peroxynitrite in the stimulation of apoptosis has been considered. Bonfoco et al. [144] has found that the producers of low peroxynitrite concentrations during the exposure of cortical neurons to the low level of NMDA or the use of peroxynitrite donors resulted in an apoptosis in neurons, while the high concentrations of peroxynitrite induced necrotic cell damage. The formation of peroxynitrite is apparently responsible for NO-stimulated apoptosis in superoxide-generating transformed fibroblasts because nontransformed cells, which do not produce superoxide, were not affected by nitric oxide [145]. It is of interest that proapoptotic effect of peroxynitrite may depend on the cell type. Thus, the formation of peroxynitrite enhanced the NO-induced apoptosis in glomerular endothelial cells, while superoxide inhibited the formation of ceramide and apoptosis in these cells exposed to nitric oxide probably due to peroxynitrite formation... 

Ventura, A.C., Bohnke, M. Pentoxifylline influences the autocrine function of organ cultured donor corneas and enhances endothelial cell survival. Br J Ophthalmol 85(9), 1110-1114(2001)... 

Struck, A. T., Hogg, N., Thomas, J. P., and Kalyanaraman, B., 1995, Nitric oxide donor compounds inhibit the toxicity of oxidized low-density lipoprotein to endothelial cells, FEBS Lett. 361 291-294. 

Hyperacute form Transplant rejection may occur as an antibody-related complication within a short period of time after LT. This rare event is caused by donor antigens coming into contact with preformed antibodies in the recipient, which results in damage to the endothelial cells of the arteries with vascular occlusion. The outcome is necrosis of the transplant. 

Treatment with G-CSF in 26 healthy donors for 5-7 days produced transient changes in endothelial cell and clotting activation markers (45). Although these abnormalities may indicate a risk of thrombotic complications, their clinical relevance to healthy donors is unknown. 

Hyperacute rejection may occur when preformed donor-specific antibodies are present in the recipient at the time of the transplant and may be evident within minutes of the transplant procedure. Hyperacute rejection can be induced by immunoglobulin G (IgG) antibodies that bind to antigens on the vascular endothelium, such as class I MHC, ABO, and vascular endothelial cell antigens. Tissue damage can be mediated through antibody-dependent, cell-mediated cytotoxicity or through activation of the complement cascade. The ischemic damage to the microvasculature rapidly produces tissue necrosis. 

Mesenchymal stem cells are another group of adult stem cells that have been suggested as potential donor cells (see Part I, Chapter 13). These cells are accessible from the bone marrow and peripheral blood, allow autologous transplantation, may be multipotent, and can also differentiate into specialized tissues, including possibly cardiomyocytes, endothelial cells. 

It seems prudent to conclude that transplanted early human and pig kidney precursors develop as chimeric organs in which blood vessels are of both donor and host origin, while external vessels required for graft maintenance are mostly host-derived. The exact relationship between donor- and host-derived endothelial cells in the formation of the microcirculation is currently unknown. 

In the already cited articles, NO is produced by NO donors. It can be produced by iNOS activity in macrophages [120, 121], polynuclear cells [122] or endothelial cells [123], which provokes tumor cells apoptosis. NO can also be produced by tumor cells iNOS. When iNOS gene is activated by cytokines IFNy and IL-ip in rat colon cancer cells, IFNy, IL-ip, TNFa in human colon cancer cells, TNFa in murine colon cancer cells, IL-la in human ovarian cancer cells, NO has no apoptotic effect. 

In an other hand, NO inhibits iNOS expression. When NO provokes the p53 accumulation, this one could in return inhibit iNOS gene transcription [154], Repression is observed in DLD-1 cells (human colon carcinoma) or Calu 6 cells (human pulmonary carcinoma) which express wild type p53. High NO concentration leads to p53 nitrosylation and inhibits the repression [114]. The wild type but not the mutated or the nitrosylated protein binds the iNOS gene promoter. Moreover, exogeneous NO produced by NO donors can inhibit NFkB activity in whole cells and in acellular preparation [155-157]. Those results have been confirmed in endothelial cells in which NO produced by eNOS inhibits NFkB activity and iNOS gene transcription [158], The inhibition can be explain in parts by NFkB sub-unit p50 nitrosylation [155], but also by its cytoplasmic inhibitor protein IxBa stabilisation (IkB proteins functionally retain NF-... 

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