1,720,971 research outputs found
Long pentraxin-3 modulates the angiogenic activity of fibroblast growth factor-2
No full textAngiogenesis, the process of new blood vessel formation from pre-existing ones, plays a key role in various physiological and pathological conditions. Alteration of the angiogenic balance, consequent to the deranged production of angiogenic growth factors and/or natural angiogenic inhibitors, is responsible for angiogenesis-dependent diseases, including cancer. Fibroblast growth factor-2 (FGF2) represents the prototypic member of the FGF family, able to induce a complex “angiogenic phenotype” in endothelial cells in vitro and a potent neovascular response in vivo as the consequence of a tight cross talk between pro-inflammatory and angiogenic signals. The soluble pattern recognition receptor long pentraxin-3 (PTX3) is a member of the pentraxin family produced locally in response to inflammatory stimuli. Besides binding features related to its role in innate immunity, PTX3 interacts with FGF2 and other members of the FGF family via its N-terminal extension, thus inhibiting FGF-mediated angiogenic responses in vitro and in vivo. Accordingly, PTX3 inhibits the growth and vascularization of FGF-dependent tumors and FGF2-mediated smooth muscle cell proliferation and artery restenosis. Recently, the characterization of the molecular bases of FGF2/PTX3 interaction has allowed the identification of NSC12, the first low molecular weight pan-FGF trap able to inhibit FGF-dependent tumor growth and neovascularization. The aim of this review is to provide an overview of the impact of PTX3 and PTX3-derived molecules on the angiogenic, inflammatory, and tumorigenic activity of FGF2 and their potential implications for the development of more efficacious anti-FGF therapeutic agents to be used in those clinical settings in which FGFs play a pathogenic role
Vascular oxidative stress-induced senescence is minimized by melatonin intake in Apo-E deficient mice
Full text linkAging is a natural process that produces deleterious changes in all tissues of the organism. One leading theory about the cause of aging suggest that oxidative stress play a fundamental role in pathogenesis. Oxidative stress induces intracellular damage that affects all biological components, including, DNA, lipids, sugars and proteins. Therefore, the imbalance between intracellular reactive oxygen species (ROS) and antioxidant defence mechanisms results in harmful oxidative stress. One of the most widely considered strategies for preventing aging and for treating age-related disease is the use of natural anti-oxidant agents, such as melatonin and resveratrol. Melatonin is a potent endogenous anti-oxidant neurohormone, which acts through various mechanisms to ameliorate the toxic effects of ROS. However, little is known about the mechanisms of signalling pathways through which melatonin acts to reverse the effects of ROS. In the present study we treated ApoE-deficient mice, a well-known senescence model, from 6th week to 15th week of life, with a specific melatonin formulation: Armonia Retard (kindly provided by Nathura s.r.l, Reggio Emilia, Italy), with an extended-release pharmacokinetic, at different progressive doses 0.04, 0.1, 10 mg/kg/day. We used the same treatment in C57BL6 mice, as control group. Vascular alterations were evaluated in aorta by morphology and immunofluorescence analysis was focused on pleiotropic inflammatory markers, such as interleukins (IL) 6 and 10, inducible nitric oxide synthase (iNOS), tumor necrosis factor-alpha (TNF-α). We observed in ApoE-deficient mice endothelial cell detachment and IL-6, IL-10, iNOS and TNF-α overexpression. Melatonin treatment improved not only the endothelial damage, but also the overall vascular cytoarchitecture and reduced inflammation and macrophages infiltration. In particular, melatonin Retard at the highest dose, recovered all the above markers to the levels of C57BL6 mice. These results outline the anti-inflammatory and anti-oxidant properties of melatonin and its beneficial anti-aging and anti-atherosclerotic effects, especially in extended-release formulation
Upregulation of HO-1 accompanied by an increase in adiponectin improves cardiac function via Pamp-Penos pathway in spontaneously hypertensive rats.
No full textGoing 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
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