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Biomedical subjects

F Ghezzo

Publications and source records attributed to F Ghezzo.

At least 19 recordsLinked to original sources
PubMed1989

Identification of serum-responsive elements in the promoter of human calcyclin, a growth-regulated gene.

The calcyclin gene is growth regulated in a number of cell types from different animal species. We have identified in the promoter region of the human calcyclin gene the sequences responsible for its growth regulation by serum. A number of deletion mutants and synthetic nucleotides, all driving the chloroamphenicol transferase (CAT) gene, were constructed for this purpose. Serum-responsive elements can be localized in the last 42 bp immediately upstream from the CAP site.

Animals↗
PubMed1988

Growth factor regulation of the promoter for calcyclin, a growth-regulated gene.

The steady-state levels of calcyclin mRNA are regulated by growth factors. Using deletion mutants of the 5'-flanking region and a linked reporter (the bacterial chloroamphenicol transferase gene), we have investigated the elements of the calcyclin gene's promoter that respond to growth factors. By a transient expression assay after transfection in BALB/c/3T3 cells, we have been able to show that the serum-inducible sequences are contained in a 164-base pair fragment just upstream of the cap site. This fragment also contains an enhancer, and responds to platelet-derived growth factor as well as to serum. The sequences from -1371 to -1194 upstream of the cap site contain an element which is negatively regulated by epidermal growth factor. These findings have been confirmed in hamster cell lines in which the deletion mutants of the calcyclin promoter controlled the expression of the cDNA for human thymidine kinase. These results indicate that, like in other growth-regulated genes the activity of the calcyclin promoter is modulated by both positive and negative elements. Even more intriguing, though, is the finding that some of these negative elements may be influenced by growth factors in the environment.

Animals↗
PubMed1987

Structural and functional analysis of a growth-regulated gene, the human calcyclin.

Calcyclin was originally defined as a cDNA clone (2A9) whose cognate RNA is growth-regulated and whose sequence shows strong similarities to the sequences of the S-100 protein, a calcium-binding protein, as well as to a subunit of the major cellular substrate for tyrosine kinase. Using the full-length cDNA, we have now isolated from a human genomic library several phages containing calcyclin sequences. One of the phages, ch. 28-10, contains the entire calcyclin gene, plus extensive flanking sequences. The calcyclin gene is a unique copy gene and has 3 exons. The 5' flanking sequence has been characterized, both structurally and functionally. Besides a TATA box, it contains, in the region proximate to the cap site, GC boxes and a sequence with a strong homology to the enhancer core of the SV40 promoter. Other enhancer-like elements are found scattered in both the 5' and 3' flanking regions. The proximate 5' flanking region is very active in driving the transient expression of linked reporters in transfection experiments. Finally, the calcyclin gene has been localized to the long arm of human chromosome 1, near the ski oncogene.

Base Sequence↗
PubMed1987

Heparin neutralizes serum antiplasmin inhibition of peripheral blood leukocyte fibrinolytic activity.

Serum inhibition of peripheral blood fibrinolytic activity has been evaluated with the 125I-fibrin coated well method. The inhibitory activity was found in a 140,000 d serum fraction that contained alpha 2-antiplasmin. Addition of heparin to cell cultures at concentrations in the range of values obtained during anticoagulant therapy has been demonstrated to counteract such inhibitory activity. The phenomenon has been shown to be linked with plasminogen activation in the presence of fibrin, to lead to a weakening of antiplasmin activity. By clarifying an important aspect of the mechanism of heparin action, our findings support the view that heparin can be usefully employed in treating thrombotic syndromes, not only as an anticoagulant, but also as a "profibrinolytic" agent.

Fibrin↗
PubMed1987

[Lymphocyte subpopulations in idiopathic dilatational cardiomyopathy].

Lymphocyte subsets have been examined in 23 patients affected by idiopathic dilated cardiomyopathy (IDCM). Patients were divided according to their functional class showing that compromised subjects exhibited high T-lymphocyte helper/suppressor ratio whereas the contrary was observed in the other patients. It has therefore suggested that IDCM is characterized by 2 distinct phases, each of them with different helper/suppressor ratio.

Adult↗
PubMed1986

Interaction between leukocytes and serum plasminogen: an essential mechanism in peripheral blood fibrinolytic activity.

Intense fibrinolytic activity (FA) by granulocytes, mononuclear adherent cells, and natural killer (NK) cells was demonstrated by using 125I-fibrin-coated wells. This FA was greatly dependent on serum plasminogen, provided that serum inhibitors were destroyed by heating at 56 degrees C. Using monoclonal antibodies, it was also observed that these leukocytes produce urokinase and that this enzyme is secreted during adhesion by mononuclear adherent cells and during the cytotoxicity reaction against neoplastic cells by NK cells. Since cell intactness is necessary for leukocyte-serum interaction, stress is placed on the membrane function. We conclude that leukocytes are essential in peripheral blood FA and that transport of urokinase by circulating cells, inside their cytoplasm, could offset its lack of affinity for fibrin and thus avoid undesirable systemic effects.

Cell Adhesion↗
PubMed1983

Insulin modulates human mononuclear adherent cell fibrinolytic and phagocytic activities.

The effects of physiological concentrations of insulin on the fibrinolytic activity of peripheral blood leucocytes were investigated. Significant enhancement of the fibrinolytic activity of mononuclear adherent cells was observed, whereas lymphocytes and granulocytes were unaffected. Furthermore, insulin stimulated mononuclear adherent cells to phagocytize inert particles but not to secrete lysozyme. It is suggested that these results are attributable to the large number of insulin receptors present on the monocyte membrane, and that the regulatory mechanism of fibrinolysis and phagocytosis differs from that controlling the secretion of lysozyme.

Cell Adhesion↗
PubMed1982

[Phagocytic activity and cytochemical characterization of acute human myeloblastic leukemia cells].

The ability of leukemic cells to phagocytize in vitro inert latex particles was tested in a group of non-lymphoblastic acute leukemia causes classified according to the FAB criteria. Promyelocytic, myelomonocytic, and myeloblastic leukemias were found to possess the highest percentage of cells with phagocytic activity. The cytochemical characterization of the cells revealed that the majority of phagocytic elements were negative for alpha-naphtyl acetate staining and positive for the peroxidase reaction. These unexpected findings could be explained by the impaired differentiation process of leukemic cells.

Humans↗
PubMed1982

[Effects of insulin on fibrinolytic and phagocytic activity of peritoneal macrophages in mice].

The effects of insulin on the in vitro fibrinolytic activity and on the ability to ingest inert latex particles of murine peritoneal macrophages were studied. The addition to the cell cultures of insulin at the concentration of 25 ng/ml significantly increased both fibrinolytic and phagocytic activities. These findings suggest that insulin may play an important role not only in the regulation of the cellular metabolic process but that also directly modulates specific cell functions.

Animals↗
PubMed1982

Release of platelet-activating factor from HL-60 human leukemic cells following macrophage-like differentiation.

Platelet-activating factors (PAF), a phospholipid mediator of anaphylaxis, is also known to be released in vitro from both phagocytic polymorphonuclear neutrophils (PMN) and monocytes in response to a variety of stimuli. The fact that human myeloid cells of the HL-60 line can be made to differentiate in vitro into macrophage-like cells by 12-O-tetradodecanoylphorbol-13-acetate (TPA) prompted us to investigate the generation and release of PAF during this transformation. Both passive release of PAF at pH 9.5, and active release, following phagocytosis of C3b- and C3d-opsonized yeast spores, and stimulation with C5a anaphylatoxin from untreated and TPA-treated HL-60 cells, PMN, and plastic-adherent normal human monocytes were studied. It was found that after 3 days of TPA treatment, HL-60 cells released PAF following phagocytosis of C3b- and C3d-opsonized yeast spores. Inhibition of PAF release by a selective inhibitor of phospholipase A2 and labeling of PAF with sodium 14C-acetate indicated that PAF generation is a two-step process: (1) release of PAF precursor from cell membranes and (2) its acetylation. A model for the in vivo study of mechanisms and metabolic events involved in PAF generation and release could perhaps be built on these findings.U

Cell Line↗
PubMed1981

Effects of aspirin treatment upon fibrinolytic activity of peripheral blood granulocytes.

The effects of in vivo acetylsalicylic acid (ASA) treatment on the fibrinolytic activity of peripheral blood granulocytes have been studied in a group of healthy volunteers. Following a 4-day treatment with aspirin at a dose of 1 g/day, both the plasminogen-dependent and the nonspecific fibrinolytic activity were significantly decreased. On the contrary, no significant change in the granulocyte fibrinolytic activity was found after treatment with 250 mg ASA/day. It is suggested that the cellular release mechanism of such lytic enzymes rather than their synthesis could have been affected by the drug.

Adolescent↗
PubMed1981

[The biological action of dithiocarbamates. Changes in serum leucine aminopeptidase induced in vitro by sodium diethyldithiocarbamate].

The Authors demonstrate that serum LAP activity in vitro is inhibited by NaDDTC. This may be related to the NaDDTC chelating-like action on the metallo-enzyme. The trend of the phenomenon follows an exponential pattern. The enzyme activity was completely restored after removal of NaDDTC from the medium by dialysis. The NaDDTC concentration able to inhibit the enzymatic activity in vitro was much higher than in vivo, in experimental animals. The Authors conclude pointing out the problem of a probable effect caused by repeated doses of dithiocarbamates more on enzyme synthesis than on metallic apoenzyme.

Animals↗