Search PubMed⌕ Search

Biomedical subjects

M Aglietta

Publications and source records attributed to M Aglietta.

At least 109 records · Page 6Linked to original sources
PubMed1984

Differences in the in vitro growth pattern of fresh and cryopreserved granulo-monopoietic precursors.

A study of the in vitro growth model of human granulo-monopoietic precursors (CFU-GM) before and after cryopreservation using both leukocyte feeder layers and GCT conditioned medium as the source of colony stimulating activity (CSA) is reported. The number of colonies produced with fresh cells was linearly related to the amount of marrow seeded with both CSA sources, whereas after cryopreservation this was true with feeder layers, and with GCT only at relatively high cell concentrations. This might indicate the production of granulopoietic stimulators on the part of a second population that is at least partly resistant to freezing. It seems more likely, however, that these results depend mainly on a sublethal damage to CFU-GM induced by freezing, thus making the cells hyporesponsive to some forms of CSA, such as those contained in GCT conditioned medium.

Cell Division↗
PubMed1984

Retinoic acid enhances the growth of only one subpopulation of granulomonocyte precursors.

The effect of various concentrations of retinoic acid on the growth of committed granulomonopoietic precursors (CFU-GM) was studied on semisolid agar cultures. Retinoic acid increased the growth of day 14 CFU-GM but had no significant effect on day 7 CFU-GM. Since the latter are believed to represent the progeny of day 14 CFU-GM it is suggested that the effect of retinoic acid is confined to the early stages of granulomonocytic differentiation.

Bone Marrow Cells↗
PubMed1984

An in vitro study of basophil production in chronic myeloproliferative disorders.

An examination was carried out of certain parameters of basophil production in semisolid agar cultures by granulomonocyte precursors (CFU-C) from normal subjects and from patients with chronic myeloproliferative disorders. Basophils were rare in the first four days of culture, after which their number increased gradually to reach a plateau on about the 12th day. Pure basophil colonies were frequent only in cultures from a patient with marked basophilia. In the other cases the colonies also included other cells of the granulomonocyte pathway. There was a linear correlation between basophilia in vivo and basophil production in vitro. The latter, however, was influenced by the type of colony-stimulating activity (CSA) used. Different CSA sources, inducing the production of a comparable number of colonies, did not stimulate basophilic differentiation in the same way. Serum from patients with chronic myelocytic leukemia and varying degrees of basophilia did not have a significant effect on autologous in vitro basophilopoiesis, nor did it increase that of normal CFU-C.

Basophils↗
PubMed1983

Responsiveness to prostaglandin E1 of different subtypes of normal and pathological committed granulomonopoietic precursors.

The influence of prostaglandin E1 (PGE1) on colonies produced by different subtypes of committed granulomacrophagic precursors (CFU-GM) was studied. Even though they represent a more immature class of precursors than day 7 CFU-GM, day 14 CFU-GM have the same sensitivity to PGE1: their growth is significantly inhibited by low PGE1 concentrations (10(-10) M or higher). Macrophagic colony formation is most sensitive to PGE1. Pure granulocytic colonies are relatively resistant and significantly inhibited by high concentrations only. Mixed granulomacrophagic colonies display an intermediate degree of sensitivity. Both day 7 and day 14 CFU-GM from chronic myeloid leukemia and idiopathic myelofibrosis patients are significantly less sensitive than normal CFU-GM. This insensitivity is not dependent on a lack of production of macrophagic colonies, since these may even be present in a higher than normal frequency.

Alprostadil↗
PubMed1983

Biosynthesis and release of platelet-activating factor from human monocytes.

The aim of the present study was to investigate the pathways of platelet-activating factor (PAF) production and release from human monocytes. For this purpose, both phagocytic stimuli and stimuli induced by soluble agents were used. The phagocytic stimuli exerted their effect in a receptor-specific mechanism related to surface Fc, C3b and C3d receptors. Stimuli induced by soluble agents, such as A23187 and pH 10.6, which do not require interaction with specific receptors, were also effective in inducing PAF release. In contrast, C5a, a soluble agent which induces a receptor-mediated release of PAF from neutrophils, failed to induce PAF release from monocytes. PAF release from monocytes could be dissociated from phagocytosis and from release of lysozyme. The PAF release required the presence of extracellular cations, the activation of membrane esterase and phospholipase A2 and the integrity of the microfilament system. Moreover, PAF release was modulated by lipoxygenase and intracellular cAMP levels. The relevance of an acetylation process in the biosynthesis of PAF was suggested by the increase of PAF yields in the presence of sodium acetate and by the incorporation of 14C-sodium acetate into molecules of active PAF.

Acetates↗
PubMed1983

The release of platelet-activating factor from human endothelial cells in culture.

The release of platelet-activating factor (PAF) from stimulated human endothelial cells (HEC) cultured from normal term, umbilical cord veins is described. HEC in primary cultures released PAF after challenge with A23187, rabbit anti-human factor VIII (RaHu/FVIII), angiotensin II, and vasopressin. HEC subcultures maintained the ability to release PAF in the presence of A23187 and RaHu/FVIII, whereas the release of PAF in response to angiotensin II and vasopressin was not constant and was reduced. Control cultured, smooth muscle cells derived from umbilical cord veins, previously depleted of endothelial cells, did not release PAF under the above-mentioned stimulation. Plastic-adherent or cultured monocytes released PAF with A23187, but not with RaHu/FVIII, angiotensin II, and vasopressin. The release of PAF from HEC in primary cultures required the presence of extracellular cations and the activation of membrane phospholipase A2. PAF release induced by A23187, RaHu/FVIII, angiotensin II, and vasopressin was unaffected by indomethacin, an inhibitor of cyclooxygenase, which, however, favored the release of PAF from HEC stimulated with thrombin, a stimulus that did not affect HEC in the absence of indomethacin. PGI2 inhibited PAF release from stimulated HEC. The relevance of an acetylation process in the biosynthesis of PAF and HEC was supported by the following evidence: 1) the increase in PAF yield in the presence of sodium acetate and, particularly, of acetyl-CoA; 2) the incorporation of [14C]acetate into PAF molecules; 3) the loss of radioactivity and of biologic activity after treatment with phospholipase A2. These results indicate that HEC in culture are able to release PAF and that metabolic pathways similar to those described for leukocytes are involved.

Angiotensin II↗
PubMed1981

Release of platelet-activating factor (PAF) and histamine. II. The cellular origin of human PAF: monocytes, polymorphonuclear neutrophils and basophils.

The origin of platelet activating factor (PAF) from human leucocytes was investigated. Purified monocytes release PAF passively at pH 10.6, when challenged with Ionophore A 23187 or under phagocytic stimuli. Pure preparations of polymorphonuclear neutrophils liberate PAF passively, when challenged with C5a, neutrophil cationic proteins (CP), their carboxypeptidase B derived products (C5a des Arg, CP des Arg) or under phagocytic stimuli. Basophil rich buffy coat cells release PAF when challenged with C5a, CP, anti-IgE (in low amount) or Synacthen concomitantly with basophil degranulation and histamine release. Electron microscopy studies, carried out on Synacthen-stimulated basophil rich buffy coat, provide morphological evidence for platelet-basophil interaction. In conclusion our data demonstrate that PAF can be released from different leucocyte populations. However, the stimuli able to trigger such release appear to have some specificity for the cell target.

Antigen-Antibody Complex↗
PubMed1981

Detection of basophils growing in semisolid agar culture.

The production of basophils in semisolid agar cultures form normal and chronic myeloid leukemia (CML) committed granulocyte-macrophage precursors was investigated using an original whole-dish staining technique with toluidine blue which produces a specific metachromasia in basophils. As additional proof of the basophilic nature of metachromatic cells, their degranulation after challenge with C5a anaphylotoxin and Synachten was observed. Our studies show that few basophils are produced in cultures form normal bone marrow. CML CFUc produce more basophils, their number being roughly correlated with the degree of basophilia. We observed only clusters composed by a pure basophilic population, while larger aggregates in which basophils could be detected were composed also by other granulocytic cells.

Agar↗
PubMed1980

Different kinetic pattern of chronic myeloid leukemia: lymphoblastic and myeloblastic blastic crisis.

Cell kinetic studies were performed in 8 case of lymphoid blastic crisis (BC) of chronic myeloid leukemia at the onset of BC and during subsequent relapses. The results were compared with those found in 7 myeloblastic BC. While in the myeloblastic transformation the labeling index (LI) was always higher in bone marrow than in peripheral blood blasts, suggesting a predominant bone marrow proliferation of the leukemic cells, in the lymphoid transformation a higher LI was often found in peripheral blasts. Moreover, the lymphoblastic transformations were frequently characterized by lymphadenopathy. These findings point to the similarities between lymphoid BC and acute lymphoblastic leukemia, suggesting the possibility that a blastic event may originate in an extramedullary site and that an extramedullary BC is more likely to be lymphoid in nature.

Adult↗
PubMed1980

Insensitivity of chronic myeloid leukemia cells to inhibition of growth by prostaglandin E1.

The influence of E prostaglandins on the in vitro growth of chronic myeloid leukemia (CML)-committed granulopoietic precursors [colony-forming unit-culture (CFU-C)] has been investigated in a double-layer agar system in which CFU-C growth was stimulated by adherent monocytes. Addition of the prostaglandin synthesis inhibitor indomethacin to the feeder layer significantly increased the number of normal CFU-C, whereas CML CFU-C were unaffected. Exogenous prostaglandin E1 inhibited CML CFU-C growth at concentrations 1000-fold higher than those necessary to produce a similar effect on normal CFU-C. These data point to a lower than normal sensitivity of CML-committed granulopoietic precursors. It is suggested that derangement of the responsiveness of CML cells to prostaglandin regulation may play a role in the pathogenesis of uncontrolled leukemic proliferation.

Bone Marrow↗