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      Effect of the Hemodialysis Session on bcl-2 Expression in Peripheral Blood Mononuclear Cells in vivo

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          bcl-2 is a proto-oncogene with a regulatory role in many conditions due to its marked inhibitory action on apoptosis. Reports regarding the effect of hemodialysis (HD) on apoptosis of mononuclear cells and in association with bcl-2 expression in particular, are controversial. The aim of the present study was to examine in vivo the influence of an HD session on bcl-2 expression of lymphocytes and monocytes. We measured quantitative bcl-2 expression with flow cytometry, in terms of antibodies bound per cell, in blood samples taken from 44 HD patients before and after an HD session. 27 patients (group I) were dialyzed with synthetic-type membranes and 17 (group II) with cellulose-type membranes. bcl-2 expression increased statistically significantly in lymphocytes (1,616 ± 718 to 1,894 ± 715 molecules/cell, p < 0.01) at the end of HD. Monocyte expression of bcl-2 was lower than in lymphocytes and almost did not change after the HD session (654 ± 446 to 698 ± 375 molecules/cell, p = NS). Comparison between the two groups did not reveal a significant difference in either the baseline bcl-2 expression or in the value of the increase after HD. We conclude that HD seems to decrease lymphocyte apoptosis independent of the biocompatibility of the dialyzer membrane.

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          Most cited references 15

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          Bcl-2 functions in an antioxidant pathway to prevent apoptosis.

          Bcl-2 inhibits most types of apoptotic cell death, implying a common mechanism of lethality. Bcl-2 is localized to intracellular sites of oxygen free radical generation including mitochondria, endoplasmic reticula, and nuclear membranes. Antioxidants that scavenge peroxides, N-acetylcysteine and glutathione peroxidase, countered apoptotic death, while manganese superoxide dismutase did not. Bcl-2 protected cells from H2O2- and menadione-induced oxidative deaths. Bcl-2 did not prevent the cyanide-resistant oxidative burst generated by menadione. Two model systems of apoptosis showed no increment in cyanide-resistant respiration, and generation of endogenous peroxides continued at an inherent rate that was unaltered by Bcl-2. Following an apoptotic signal, cells sustained progressive lipid peroxidation. Overexpression of Bcl-2 functioned to suppress lipid peroxidation completely. We propose a model in which Bcl-2 regulates an antioxidant pathway at sites of free radical generation.
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            Apoptosis in development.

            Essential to the construction, maintenance and repair of tissues is the ability to induce suicide of supernumerary, misplaced or damaged cells with high specificity and efficiency. Study of three principal organisms--the nematode, fruitfly and mouse--indicate that cell suicide is implemented through the activation of an evolutionarily conserved molecular programme intrinsic to all metazoan cells. Dysfunctions in the regulation or execution of cell suicide are implicated in a wide range of developmental abnormalities and diseases.
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              B lymphopenia in uremia is related to an accelerated in vitro apoptosis and dysregulation of Bcl-2.

              Lymphopenia has been described in patients with chronic renal failure (CRF). It is postulated that the decline in lymphocytes is due to accelerated apoptosis. We investigated whether dysregulation of programmed cell death plays a role in the immunodeficiency described in CRF. Peripheral blood lymphocytes (PBL) from pre-dialysis uraemic patients (nHD) and haemodialysed patients (HD) were cultured with no stimulus for 96 h. Apoptosis of lymphocytes was measured by propidium iodide staining and flow cytometry. Expression of Fas and Bcl-2 was also analysed by flow cytometry. Peripheral blood B cells were significantly lower in pre-dialysis and haemodialysis uraemic patients compared to control. Lymphocytes from both groups of patients had a higher rate of apoptosis in vitro than those from healthy controls. This effect was more pronounced in B lymphocytes and a significant correlation between the B lymphopenia and the percentage of apoptotic B cells after 48 h of culture without stimulus was observed. The increased lymphocyte apoptosis in CRF was accompanied by a significantly lower in vitro Bcl-2 expression. However, Fas did not seem to play a role in spontaneous lymphocyte apoptosis in end-stage renal disease. Our data indicate that B lymphopenia in CRF may be partially attributed to an increased susceptibility to cell death by apoptosis that is associated with a decreased expression of Bcl-2.

                Author and article information

                Blood Purif
                Blood Purification
                S. Karger AG
                December 2006
                21 December 2006
                : 24
                : 5-6
                : 542-547
                aDepartment of Nephrology and Hematology Laboratory, and bMolecular Biology Unit, University Hospital of Ioannina, Ioannina, Greece
                97077 Blood Purif 2006;24:542–547
                © 2006 S. Karger AG, Basel

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                Figures: 3, Tables: 2, References: 22, Pages: 6
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