1,721,050 research outputs found
Terminal transferase positive rat thymocytes are resistant to steroid-induced apoptosis.
Full text linkApoptosis is a prominent mechanism of programmed cell death in the immune system. In the thymus apoptosis is responsible for the deletion of autoreactive T-cells during thymic differentiation. The typical features of apoptosis are characterized by nuclear and cytoplasmic morphologic changes, along with cleavage of chromatin at regularly spaced sites. Terminal deoxynucleotidyl transferase (TdT) is a DNA polymerizing enzyme found at an early stage of T and B lymphocyte differentiation, which generates diversity in the DNA sequence of immunoglobulin (Ig) or T cell receptor (TCR). The combined evaluations of thymocyte morphological features, immune phenotype and thymic topography associated to TdT expression allow the recognition of three different thymocyte subpopulations, characterized by small-size, intermediate-size and large-size. The results of this study show that dexamethasone (Dx)-treatment induces cell death via apoptosis involving distinct transformations related to differentiation stages of thymic subpopulations. Intermediate and small-size thymocytes that are TdT-negative or weakly positive at nuclear level are Dx sensitive. In contrast the large-size thymocytes, highly TdT positive, corresponding to the undifferentiated cells, do not show significant morphological modifications and TdT positivity to Dx-treatment. Immunocytochemical analysis shows that Dx-treatment does not affect TdT synthesis but morphological changes, occurring during apoptotic process, are responsive to intracellular movement and intranuclear arrangement of the TdT
Interferon-gamma (IFN-gamma) induces programmed cell death in differentiated human leukemic B cell lines.
No full textInterferons (IFNs) are cytokines that exert an antiviral effect on target cells and possess immunomodulatory and antitumor properties. In this study we have investigated the effects of human recombinant IFN-gamma on human leukemic B cell lines at different stages of maturation. Our data show that in Burkitt's lymphoma RAMOS-1 B cells IFN-gamma induces a reduction of cell growth and a clonal selection via programmed cell death; in contrast, IFN-gamma treatment of KM-3 pre-B cells does not induce biochemical and morphological changes as shown by electron microscope analysis and DNA gel electrophoresis
Intracellular localization of terminal transferase during the cell cycle.
No full textChanges in the localization of terminal transferase during the cell cycle in random cultures of human pre-T leukemia line RPMI-8402 were examined by light and electron microscopy on immunoperoxidase-stained preparations. Paraformaldehyde-fixed and saponin-permeabilized human cells were used with a monoclonal anti-human terminal deoxynucleotidyl transferase (TdT) primary reagent to demonstrate changes in enzyme distribution occurring between interphase and mitosis. Nuclear localization is found uniformly during interphase. At metaphase, however, the majority of TdT staining appears randomly distributed in the cytoplasm and traces of TdT staining remain associated with mitotic chromatin. At later phases, when the daughter cells are forming, the enzyme again appears to be restricted to the new nuclear structure
Dimethyl sulfoxide induces programmed cell death and reversible G1 arrest in the cell cycle of human lymphoid pre-T cell line.
No full textProgrammed cell death of peripheral myeloid precursor cells in Down patients: effect of zinc therapy.
No full textThe c-myc gene regulates the polyamine pathway in DMSO-induced apoptosis.
No full textIt is accepted that apoptosis is a gene-controlled process of cellular self-destruction. It occurs during physiological regulation and in pathological situations in the life of a cell. In the immune system, several different intracellular and extracellular factors have been associated with the induction of apoptosis, and the final responses depend on the cell system and the acquired signals. In lymphoid cells, dexamethasone-induced apoptosis is associated with c-myc downregulation in cells that remain in G0-G1 until the point of death. Ornithine decarboxylase (ODC), a key enzyme involved in polyamine biosynthesis, is regulated by c-myc, which is a transcriptional activator implicated not only in the control of cell proliferation and differentiation but also in programmed cell death. As dimethylsulphoxide (DMSO) induces apoptosis in the RPMI-8402 human pre-T cell line, the present study analysed the involvement of the c-myc proto-oncogene and polyamine pathway as mediators of apoptosis. Cell growth, programmed cell death, c-myc expression, ODC activity and intracellular polyamine content were detected after DMSO and difluoromethylornithine (DFMO) treatment. DMSO-treated cells exhibit a decrease in ODC activity and polyamine levels associated with cell growth arrest and programmed cell death induction. The expression of c-myc proto-oncogene, as its mRNA or protein, is specifically down-regulated. DFMO, a well defined polyamine biosynthesis inhibitor, completely blocks ODC activity, resulting in growth inhibition but not apoptosis. Moreover, in these samples no evidence of changes of c-myc expression were found. The results obtained suggest that, in RPMI-8402 cells, DMSO provokes a c-myc-dependent decrease of ODC activity followed by a depletion of intracellular polyamine levels, associated with programmed cell death and cell growth arrest
Phorbol ester synergizes the dimethyl sulfoxide-dependent programmed cell death through diacylglycerol increment.
No full textThe regulation of cell proliferation or cell death by extracellular factors are the most intensely studied subjects in cell biology. Many conceptual problems remain to be clarified concerning the mechanisms that regulate the programmed cell death. In this work, we focus our attention on the possible role of protein kinase C activation during dimethyl sulfoxide (DMSO)-induced cell death. The present results suggest that the frequency of DMSO-dependent apoptosis of RPMI 8402 thymic lymphoma cells is increased by phorbol ester acetate supplementation. Enhancement of apoptosis can be abolished by cotreatment with the bisindolylmaleimide, a specific PKC inhibitor. The association between PMA and DMSO treatment provokes an early activation of an intracellular signaling mechanism that results, via sustained diacylglycerol elevation, in a possible long-term PKC activation
Pituitary adenomas, stem cells, and cancer stem cells: what's new?
No full textPurpose
To clarify the existence of pituitary stem cells (SCs) both in the embryonic and the postnatal gland and the role for SCs in pituitary adenomas.
Methods
This work, which does not address the pathogenesis of pituitary adenomas, reviews the latest research findings and discoveries on SCs in pituitary and cancer SCs (CSCs) in pituitary adenomas and discusses the involvement of the EMT.
Results
Several groups using different approaches and techniques have demonstrated the existence of SCs and CSCs and as they are major players in pituitary adenoma onset.
Conclusions
As in other benign and malignant tumors, the hypothesis that CSCs play a pivotal role in pituitary adenoma onset has been confirmed as well as the existence of a link between the epithelial-to-mesenchymal transition (EMT) process and CSC formation in epithelial tumors
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