1,721,068 research outputs found
Patologia generale e fisiopatologia : per le professioni sanitarie
No full textIl testo è pensato per fornire agli studenti dei corsi di laurea delle professioni sanitarie le conoscenze essenziali per affrontare lo studio dell'immunologia, della patologia generale e della fisiopatologia. La nuova edizione del volume, aggiornata e arricchita, e' stata completamente ridisegnata e ripensata considerando le nuove esigenze didattiche di studenti e docenti
Magnesium and the endothelium : from the bench to the bedside
No full textContributo presentato alla sessione: Mg and the cardio-cerebrovascular system : from bench to bedside, 11 March 2008. Discussion leaders: Jeanette A. M. Maier and Rhian Touyz
Low magnesium and atherosclerosis: an evidence-based link
No full textSeveral data indicate that magnesium deficiency caused by poor diet and/or errors in its metabolism may be a missing link between diverse cardiovascular risk factors and atherosclerosis. Experimentally induced low plasma levels of magnesium accelerate atherogenesis by increasing LDL concentrations and their oxidative modifications, and by promoting inflammation. In vitro studies have shown that low magnesium determines endothelial dysfunction, the initiating event leading to the formation of the plaque. Moreover, oral magnesium therapy has been shown to improve endothelial function in patients with coronary artery disease. Magnesium, which is an inexpensive, natural and rather safe element, could be useful in preventing atherosclerosis and as an adjuvant therapy in patients with clinical manifestations of the disease
Endothelial cells and magnesium : implications in atherosclerosis
No full textThere is no doubt that the functional and structural integrity of the endothelium is critical in maintaining vascular homoeostasis and in preventing atherosclerosis. In the light of epidemiological and experimental studies, magnesium deficiency is emerging as an inducer of endothelial dysfunction. In particular, data on the effects of low extracellular magnesium on cultured endothelial cells reinforce the idea that correcting magnesium homoeostasis might be a helpful and inexpensive intervention to prevent and treat endothelial dysfunction and, consequently, atherosclerosis
Human Micro- and Macrovascular Endothelial Cells Exposed to Simulated Microgravity Upregulate hsp70
No full textMicrogravity is known to have adverse effects on the eukaryotic cells. Here we report that microgravity affects the behaviour of human micro- and macro-vascular endothelial cells. To simulate microgravity we have utilized a NASA-developed bioreactor, the Rotating Wall Vessel (RWV). Macrovascular cells proliferate faster in the RWV than controls and, accordingly, downregulate p21, which inhibits the transition from the G1 to the S phase. On the contrary, microvascular cells are growth retarded in simulated microgravity and upregulate p21. No apoptosis was detected in both the cell types. In parallel, upregulation of heat shock protein (hsp) 70 was observed in the two cell types. Because it is reported the hsp70 increases endothelial survival, we hypothesize that hsp70 induction might protect against apoptosis. Hsp70 upregulation might therefore represent an important adaptive response of human endothelial cells to simulated microgravity
Magnesium and cancer : a dangerous liaison
No full textA complex relationship links magnesium and cancer. The aim of this review is to revisit current knowledge concerning the contribution of magnesium to tumorigenesis, from transformed cells to animal models, and ending with data from human studies. Cultured neoplastic cells tend to accumulate magnesium. High intracellular levels of the cation seem to confer a metabolic advantage to the cells, contribute to alterations of the genome, and promote the acquisition of an immortal phenotype. In magnesium-deficient mice, low magnesium both limits and fosters tumorigenesis, since inhibition of tumor growth at its primary site is observed in the face of increased metastatic colonization. Epidemiological studies identify magnesium deficiency as a risk factor for some types of human cancers. In addition, impaired magnesium homeostasis is reported in cancer patients, and frequently complicates therapy with some anti-cancer drugs. More studies should be undertaken in order to disclose whether a simple and inexpensive intervention to optimize magnesium intake might be helpful in the prevention and treatment of cancer
Magnesium alloys for vascular stents: the biological bases : a focus on the effects of magnesium on vascular cells
No full textBioabsorbable vascular stents in magnesium alloys provide an attractive alternative to standard stainless steel metal stents, because of their adequate radial force, high biocompatibility, low thrombogenicity and intrinsic dissolution in body fluids. Since magnesium is the major component of the alloys, high concentrations of this element can be achieved in the local microenvironment as a results of corrosion. Magnesium is known to grant cardiovascular protection and to be beneficial for the cells of the vascular wall. This review summarizes present knowledge about the effects of high magnesium levels on smooth muscle and endothelial cells
The tyrosine phosphatase HD-PTP (PTPN23) is degraded by calpains in a calcium-dependent manner
No full textHD-PTP (PTPN23) is a non-transmembrane protein tyrosine phosphatase which contributes to the signal transduction pathways involved in the regulation of cell migration and invasion. We here demonstrate in T24 bladder carcinoma cells that HD-PTP undergoes calcium-dependent degradation which can be prevented by specific calpain inhibitors. In addition, treatment of the cells with the calpain inhibitor calpeptin results in the redistribution of endogenous HD-PTP to the periphery of the cells. Since (i) calpains are overexpressed in some tumors and (ii) the downregulation of HD-PTP enhances cell migration and invasion, we propose that HD-PTP degradation by calpains might result in the acquisition of a more aggressive phenotype in neoplastic cells
Transforming Growth Factor beta2 inhibition of Hepatocyte Growth Factor-induced endothelial proliferation and migration
No full textAngiogenesis is a highly controlled event which depends on the proper equilibrium of activators and inhibitors present within the microenvironment. Hepatocyte Growth Factor (HGF) activates migration and proliferation of endothelial cells and is angiogenic, acting through the tyrosine kinase receptor encoded by the Met protooncogene. To get insights into the molecular mechanisms involved in HGF-induced angiogenesis, we searched for cDNAs differentially expressed in human endothelial cells exposed to HGF, a potent angiogenic factor. We found that HGF-treated endothelial cells upregulated the expression of Transforming Growth Factor (TGF) β2. To understand the significance of this finding, we cultured endothelial cells with HGF and TGF β2 simultaneously. We found that TGF β2 impairs HGF-dependent proliferative and migratory responses. TGF β2 did not prevent the tyrosine phosphorylation of Met, but it inhibited some signalling pathways activated by HGF. We show that endothelial proliferation induced by HGF required the activation of the MAPK cascade, while HGF-induced endothelial migration was dependent on the tyrosine phosphorylation of Src. Indeed, TGF β2 inhibited HGF effects because it prevented HGF-induced MAP kinase activation and tyrosine phosphorylation of Src. We suggest that the induction of TGF β2 by HGF in endothelial cells may represent a physiologic mechanism to counterbalance HGF angiogenic activity
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