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F Giacchetta

Publications and source records attributed to F Giacchetta.

3 recordsLinked to original sources

Angiogenesis extent and macrophage density increase simultaneously with pathological progression in B-cell non-Hodgkin's lymphomas.

Node biopsies of 30 benign lymphadenopathies and 71 B-cell non-Hodgkin's lymphomas (B-NHLs) were investigated for microvessel and macrophage counts using immunohistochemistry and morphometric analysis. Both counts were significantly higher in B-NHL. Moreover, when these were grouped into low-grade and high-grade lymphomas, according to the Kiel classification and Working Formulation (WF), statistically significant higher counts were found in the high-grade tumours. Immunohistochemistry and electron microscopy revealed a close spatial association between microvessels and macrophages. Overall, the results suggest that, in analogy to what has already been shown in solid tumours, angiogenesis occurring in B-NHLs increases with tumour progression, and that macrophages promote the induction of angiogenesis via the release of their angiogenic factors.

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Lipoprotein (a) induces angiogenesis on the chick embryo chorioallantoic membrane.

BACKGROUND: Both lipoprotein (a) [Lp(a)] and angiogenesis have been shown to be associated with initiation and progression of atherosclerotic plaque. Lp(a) and two neutralizing anti-Lp(a) antibodies were investigated for their capacity to affect the vasoproliferative processes of the chick embryo chorioallantoic membrane (CAM), a useful model for such an investigation. METHODS: Gelatin sponges loaded with Lp(a) alone or together with anti-Lp(a) antibodies, or with vehicle alone, phosphate-buffered saline (PBS), were implanted in vivo onto the CAM at incubation day 8. Four days later, sponges and the adjacent CAM tissues were assessed for the extent of angiogenesis in terms of microvessel counts. RESULTS: Lp(a)-loaded sponges gave significantly higher counts than those loaded with the LP(a)-anti-Lp(a) antibodies complex, which overlapped those treated with PBS. The angiogenic response was similar to that obtained with basic fibroblast growth factor, a well known angiogenic molecule. CONCLUSION: These data suggest that Lp(a) is capable of inducing angiogenesis in vivo, which might account for its ability to enhance and support atherosclerosis.

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Antiangiogenesis by cyclosporine.

The effects of cyclosporine on certain endothelial cell functions, namely matrix metalloprotease (MMP)-2 and MMP-9 secretion, proliferation, chemotaxis, and morphogenesis, were investigated in vitro, and its effects on angiogenesis were studied in vivo by using the chick embryo chorioallantoic membrane (CAM) model. In vitro, at low noncytotoxic doses (2, 4, 8, and 16 microg/mL), cyclosporine inhibited all these functions in a dose-dependent manner, although MMP-2 secretion was inhibited only at 16 microg/mL. The absence of cytotoxicity was confirmed morphologically and also because inhibition was rapidly reversed as soon as cyclosporine was removed. In vivo, cyclosporine at 0.012 and 0.024 microg per CAM displayed noncytotoxic, dose-dependent antiangiogenic activity. Biochemically, the drug inhibited the activity of the endothelial cell respiratory chain enzymes succinate oxidase and cytochrome-c oxidase, again in a dose-dependent manner. This finding could explain the effects observed in vitro and in vivo. These antiangiogenic properties of low-dose cyclosporine warrant further investigation in certain autoimmune and neoplastic diseases characterized by enhanced angiogenesis.

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