1,720,987 research outputs found
PMA withdrawal in PMA-treated monocytic THP-1 cells and subsequent retinoic acid stimulation modulate the induction of apoptosis and the appearance of dendritic cells.
No full textOBJECTIVES:
To analyse proliferation, differentiation and apoptosis in THP-1 cells after stimulation with phorbol 12-myristate 13-acetate (PMA) and retinoic acid (RA).
MATERIALS AND METHODS:
PMA and RA were used in a three-step-procedure: (i) treatment with 6, 30, 60 nm PMA, that induced initial, intermediate and advanced levels of monocyte-macrophage transition, respectively; (ii) recovery in PMA-free medium; (iii) incubation with 4 μm RA. Cultures were characterized cytokinetically (flow cytometry/bromodeoxyuridine uptake) and immunocytochemically (static cytometry) for expression of CD14, CD11b (monocyte-macrophage) and DC-SIGN (dendritic cell: DCs) markers.
RESULTS:
Some treatments determined appearance of monocyte/macrophage, dendritic and apoptotic phenotypes, percentages of which were related to PMA dose used in step 1, and dependent on presence/absence of PMA and RA. PMA withdrawal induced dedifferentiation and partial restoration of proliferative activity, specially in 6 and 30 nm PMA-derived cells. Recovery in the presence of serum (fundamental to DC appearance) indicated that depending on differentiation level, cell proliferation and apoptosis were inversely correlated. Treatment with 30 nm PMA induced intermediate levels of monocytic-macrophagic differentiation, with expression of alternative means of differentiation and acquisition of DCs without using cytokines, after PMA withdrawal and RA stimulation.
CONCLUSIONS:
Our experimental conditions favoured differentiation, dedifferentiation and transdifferentiational pathways, in monocytic THP-1 cells, the balance of which could be related to both cell proliferation and cell death
Cisplatin treatment of NIH/3T3 cultures induces a form of autophagic death in polyploid cells.
No full textThe effects induced by different concentrations (50, 75, 100 microM) of the cytostatic drug cisplatin (cDDP) in NIH/3T3 cells were analyzed. Sub-confluent cultures of this mouse fibroblast line, obtained after serum deprivation, showed the presence of aneuploid/polyploid cells with ploidy values ranging from 4c to 24c. DNA content cytofluorometry demonstrated that 50 and 75 microM cDDP induced a cytostatic effect; 100 microM concentration showed lower antiproliferative action. All treatments caused a partial cell detachment and apoptosis, the incidence of which appeared to be cDDP concentration-dependent. Ultrastructural and fluorescence microscopy integrated analyses of the still adherent cells demonstrated the presence of alternative degeneration patterns, especially in polyploid cells, with extensive modifications at both nuclear and cytoplasmic levels. There were events of micronucleation and phenomena of multilobulation and furrows of the nucleus that preceded the formation of heterogeneous fragments. These events were correlated, at cytoplasmic level, with actin reorganization and the appearance of autophagocytotic processes. In our cell model, the same pharmacological treatment was able to induce different cell death phenomena relating to cell dimension and ploidy. More actively proliferating cells (2c-4c DNA content) die throughout canonical apoptosis, while polyploid cells prevailingly degenerate by mechanisms partly referable to autophagic cell death
Expression of cell kinetics and death during monocyte-macrophage differentiation: effects of Actinomycin D and Vinblastine treatments.
No full textThe different effects of two cytostatic drugs, Actinomycin D and Vinblastine, during macrophage-like differentiation induced in THP-1 monocytic cell line by phorbol ester phorbol 12-myristate 13-acetate (PMA) (6, 30, and 60 nM), were studied by morpho-cytochemical approaches. In PMA-unstimulated monocytic cells, the cytostatic effects of Actinomycin D (an antimetabolic drug) were characterized by a drastic reduction of the G2/M cells accompanied by dramatic death of the G1 cells; on the contrary, Vinblastine (a microtubule-depolymerizating drug) induced an accumulation of the G2/M cells with the appearance of aneugenic micronuclei and scarce cell death mainly from the G1 cells. After 60 nM PMA stimulation, the culture was mostly composed by macrophagic cells characterized by low proliferation and the appearance of mono-/binucleated polyploid cells; in this condition, the cytotoxicity of the two drugs, more effective for Vinblastine, induced cell death in the different ploidy classes (2c, 4c, 8c). Cell death appeared to be of apoptotic nature, but with some morpho-phenotypic differences due to the action mechanism of the drugs and dependent on cell culture growth and differentiation. As a consequence of the different block-action of the two drugs on the cell cycle phases and in relation to the different subcellular targets, the effects changed during the transition from not-adhering/proliferating monocytes to adhering/low-proliferating differentiated macrophages
Relationship between actin microfilaments and plasma membrane changes during apoptosis of neoplastic cell lines in different culture conditions.
No full textRearrangement of the microtubular network during the cell cycle phases and correlation with micronucleation and death induced by anticancer drugs in NIH/3T3 subcultures.
No full text
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Different apoptotic responses and patterns in adhering and floating neoplastic cell cultures:effects of microtubule antagonists.
No full textCellular adhesion of rat hepatocytes during the last phase of the phenotype differentiation
No full textManganese and 1-methyl-4-(2'-ethylpheny1)-1,2,3,6-tetrahydropyridine induce apoptosis in PC12 cells.
No full textOxidative stress is thought to play a key role both in the neurotoxin MPTP- and manganese (Mn)-induced neurotoxicity and in apoptotic cell death. In the present study, we report that Mn and the MPTP analogue 1-methyl-4-(2'-ethylphenyl)-1,2,3,6-tetrahydropyridine (2'Et-MPTP), which is metabolized by MAO-A to 1-methyl-4-(2'-ethylphenyl)-pyridinium ion (at concentrations of 0.5 and 1.0 mM), induced apoptosis in PC12 cells. Apoptosis was tested by terminal deoxynucleotidyl transferase-mediated 2'-deoxy-uridine-5'-triphosphate nick end labelling (TUNEL) technique, flow cytometry and fluorescence microscopy. Both Mn and 2'Et-MPTP induced also a time-dependent decrease in cell viability, as determined by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Only Mn-induced apoptosis and decrease in cell viability were inhibited by the antioxidant ascorbic acid. We conclude that apoptosis may be an important mechanism of cell death in MPTP- and Mn-induced parkinsonism. However, an oxidative stress mechanism may be recognized only in the Mn-induced apoptosis
- …
