PubMed Health⌕ Search

Biomedical subjects

M E Pasqualini

Publications and source records attributed to M E Pasqualini.

9 recordsLinked to original sources
PubMed2005

Dietary lipids modulate eicosanoid release and apoptosis of cells of a murine lung alveolar carcinoma.

Dietary arachidonic acid (AA) and eicosanoids influence neoplastic cell (NC) growth, differentiation and apoptosis. Plasma membrane fatty acid and cyclooxygenase (COX) and lipoxygenase (LOX) products were investigated in lung alveolar carcinoma cells from mice fed on different diets. Two groups were fed on a basic diet plus 6% of: corn oil (rich in 18:2n-6; CO) and on olein oil (rich in 18:1n-9; O), respectively. Control group (C) received commercial diet. NC fatty acids were analyzed by GLC, and apoptosis by flow cytometry and microscopy. In NC from CO group AA levels and LOX metabolites were increased, whereas COX metabolites decreased. NC from CO compared to O group diet showed a higher count of apoptosis and increased LOX:COX ratio. High levels of AA and decreased COX eicosanoids has been involved in anti-tumoral mechanisms by increasing tumor cell apoptosis. Present data emphasizes the implications of the dietary fatty acids on the neoplastic process in this tumoral model.

Adenocarcinoma, Bronchiolo-Alveolar↗
PubMed2003

Association between E-cadherin expression by human colon, bladder and breast cancer cells and the 13-HODE:15-HETE ratio. A possible role of their metastatic potential.

The relationship between 15(S)-HETE and 13(S)-HODE from different human tumor cells exposed to n-6 and n-3 essential fatty acids (EFAs) and E-cadherin expression was studied. Colon cancer cells (HRT-18) exposed to gamma linoleic acid (18:3n-6, GLA) and eicosapentaenoic (20:5n-3, EPA) (50microM) showed an increased expression of E-cadherin. Breast cancer (MCF-7) exposed to EPA showed an increment whereas GLA had no effect on E-cadherin expression. No expression of E-cadherin was observed for urothelial cancer (T-24) after GLA or EPA treatment. Significant levels of 15(S)-HETE and 13(S)-HODE were detected after GLA or EPA treatment for all tumor lines. E-cadherin expression was inversely proportional to the 13(S)-HODE:15(S)-HETE ratio when cells were pretreated with GLA or EPA. Nevertheless, the liberation of these metabolites seems to be independent of the E-cadherin expression. The increase in the13(S)-HODE:15(S)-HETE correlates to a decrease in the expression of E-cadherin. Both factors may play a role in metastasis development.

Arachidonic Acid↗
PubMed2000

COX and LOX eicosanoids modulate platelet activation and procoagulation induced by two murine cancer cells.

Involvement of arachidonic acid cyclooxygenase (COX) and lipoxygenase (LOX) metabolites in platelet aggregation and coagulation induced by two varieties of cancer cells of murine transplantable tumors was studied. A lung alveolar carcinoma (LAC) and a fibrosarcoma (FS), induced platelet aggregation and plasma coagulation (P<0.05). Pretreatment of both tumor lines with a COX inhibitor did not block the tumor cell induced platelet aggregation (TCIPA). COX [12(S)-HTT] and LOX [12(S)-HETE], metabolites of washed platelets (WP), alone or co-incubated with LAC or FS cells, were analyzed. We observed higher 12(S)-HETE release with respect to 12(S)HHT when WP were co-incubated with LAC cells. With both neoplastic cell (NC) lines prothrombin time (PT) was shortened. Pretreatment of NC with iodoacetic acid, soybean trypsin inhibitor or Factor X-deficient plasma increased the PT. These results indicate that AA metabolites play a role on the procoagulation and platelet aggregation induced by mesenchymal and epithelial murine cancers.

Adenocarcinoma, Bronchiolo-Alveolar↗
PubMed1997

Proaggregatory and procoagulant properties of three murine mammary gland tumor cell lines with different metastatic capabilities.

We have investigated the in vitro proaggregatory and procoagulant properties of three murine tumor cell lines having different metastatic potentials. The characterization was carried out with appropriate procoagulant inhibitors and plasma deficient in factors VII and X. The proaggregatory properties of M2, M3 and MM3 cell lines increased according to their metastatic potentials. Their procoagulant activity were dependent on factor X. The prothrombotic abilities exhibited by neoplastic cells (NC), acting synergistically, might play a role in cancer dissemination.

Adenocarcinoma↗
PubMed1994

Isologous and heterologous platelet aggregation induced by tumor cells from three murine mammary gland adenocarcinomas with different metastatic abilities.

The addition of neoplastic cells (NC) isolated from murine mammary gland adenocarcinomas having moderate and high metastatic ability on in vitro heparinized mice platelet rich plasma (PRP) induced platelet aggregation. One non-metastatic line did not induce aggregation. The aggregatory effect was not correlated with the metastatic abilities. None of the three types of tumors did cause aggregation on whole blood or PRP of rats. These adenocarcinomas seem to be suitable models to study in vitro the interactions between platelets and tumor cells having metastatic and non-metastatic potentials.

Adenocarcinoma↗
PubMed1990

Exogenous fibronectin modifies the aggregation of collagen-stimulated human platelets.

Fibronectins (FN) are adhesive glycoproteins whose role in platelet aggregation is unclear. Addition of 3, 6 and 12 micrograms/ml of human plasma FN in vitro to isolated human platelets, which had been freed from plasma FN by gel filtration and subsequently stimulated with collagen, inhibited the last stage of platelet aggregation. With 3 and 6 micrograms/ml of FN a shortening of the lag-time was also observed. These data showed that FN may play a role in platelet-collagen interaction as well as in platelet-platelet interaction.

Blood Platelets↗
PubMed1989

In vitro interaction of heterologous platelets with isolated neoplastic cells from a murine mammary gland tumor.

The purpose of the present work was to study the in vitro effects of challenging human whole-blood and platelet-rich plasma (PRP) with neoplastic cells (NC) isolated from a murine mammary gland adenocarcinoma. Viable, but not formalinized, isolated tumoral cells induced platelet aggregation in citrated whole blood. NC did not induce aggregation of PRP samples whereas the NC added to PRP induced aggregation in 33% of volunteers if samples were previously stimulated with a subaggregatory strength of collagen. The results suggest a role for other blood cells since the proaggregatory effect was less evident on PRP. Adenocarcinoma M3 seems to be a suitable model to study in vitro platelet-cell tumor interactions.

Adenocarcinoma↗
PubMedDate not supplied

Aggregatory behaviour of platelets incubated with subcellular fractions of normal and chagasic human syncytiotrophoblast.

The surface of human syncytiotrophoblast does not induce maternal blood platelet aggregation even though it is not an endothelium. It can be surmised that as occurs in endothelial injury the subcellular components of the syncytiotrophoblast may have pro- or antiaggregatory activity. During congenital Chagas' disease which is associated to trophoblast lesions, platelets may play a role in the development of T. cruzi-induced placentitis. In the present work the aggregatory behaviour of normal human blood platelets was recorded after their challenging with subcellular fractions of syncytiotrophoblast isolated from normal and chagasic women. Nuclear, Mitochondrial, Microsomal and Supernatant fractions isolated from normal and chagasic syncytiotrophoblast failed to induce per se any aggregatory reaction on platelets. When samples of platelet-rich plasma (PRP) were preincubated with normal and chagasic nuclear fractions and then stimulated with collagen at threshold level (CT-PRP) an inhibition of the aggregatory response was observed. Treatment of CT-PRP with normal and chagasic mitochondrial fractions induced inhibition of platelet aggregation whereas only chagasic fraction reduced latency time. Microsomal fraction from normal placentas showed no significant effects on platelet aggregation. It is concluded that subcellular fractions of normal human syncytiotrophoblast do not exhibit any effect on platelet aggregation, whereas those subcellular fractions enriched in intracellular membrane components isolated from chagasic placentas inhibit platelet aggregation.

Adult↗