1,721,029 research outputs found
MITOCHONDRIA AND CARDIOVASCULAR DISEASE: A BRIEF ACCOUNT
No full textMitochondria are the heart unit of the cardiac cell because they are involved in the ATP production and in the transfer to the contractile apparatus. Furthermore, mitochondria modulate Ca2+ homeostasis, manage redox status and regulate response to cellular and environmental stresses. Abnormalities in mitochondrial organelle structure and function have been observed in many cardiovascular diseases, such as ischemic cardiomyopathy, heart failure and stroke but also in drug-induced cardiomyopathies. This review summarizes the recent literature in this field
EFFECT OF ADENOSINE ON ISOPROTERENOL-INDUCED HYPERTROPHY IN VITRO. A PRELIMINARY STUDY
Full text linkPersistent β1-adrenergic stimulation is thought to induce cardiac hypertrophy, alteration in calcium regulation and Cx43 over-expression. Adenosine is a negative feedback inhibitor of adrenergic
stimulation in the heart, protecting it from toxic effects of overstimulation.
The aim of our study evaluate the effects of adenosine administration on Cx43 and pCx43 expression and [Ca2+]i in Isoproterenol-treatedcardiomiocytesby usingH9c2 cells.
Adenosine co-treatment reduced cellular hypertrophy, Cx43, pCx43 and CaMKII over-expression, and
reducedintracellularCa2+ overload.
These results suggest that the beneficial activity of adenosine on cardiomyocytes underlie the reduction
of Cx43-dependent calcium overload and CaMKII over-expression, implying a potential therapeutic in cardiac hypertrophy
Plasmacytoid Dendritic Cells Contribute to Doxorubicin-induced Tumor Arrest in a Mouse Model of Pulmonary Metastasis.
Full text linkThe biology of plasmacytoid dendritic cells (pDCs) in tumors is an emerging area of investigation. pDCs populate many human solid tumors, including lung cancer. The aim of our study was to understand the role of pDCs in pulmonary metastases during the treatment with conventional antitumor agents. For this purpose, C57Bl/6 mice were inoculated with the metastatic cell line B16-F10 or B16-Flt3L cells. The administration of doxorubicin significantly reduced the amount of pulmonary metastases in both experimental models. It is interesting to note that, 5 hours after injection, doxorubicin-induced tumor cell death was associated with higher influx of pDCs to the lung, which at 24 hours populated the mediastinal lymph nodes. In this context, lung tumor-derived pDCs obtained from mice treated with doxorubicin had higher levels of MHC I and MHC II that well correlated with the higher proliferation rate of CD4 and CD8 T cells, compared with PBS mice. Siglec-H and PD-L1 levels were not altered on lung tumor-associated pDCs derived from doxorubicin-treated and PBS-treated mice. In addition, lung tumor-associated pDCs obtained from mice treated with doxorubicin released higher levels of granzyme B. The administration of 2 consecutive doses of doxorubicin in lung tumor-bearing mice showed that B16-Flt3L-implanted mice had lower tumor burden than B16-F10-implanted mice. In conclusion, our data highlight the crucial role of the proinflammatory pDCs for the adaptive antitumor immunity. Strategies aiming at modulating pDC phenotype and activity in the tumor site might prove to be novel and effective, enhancing the conventional/actual antitumor strategies
Role of connexin 43 in cardiovascular diseases
Full text linkGap junctions (GJs) channels provide the basis for intercellular communication in the cardiovascular system for maintenance of the normal cardiac rhythm, regulation of vascular tone and endothelial function as well as metabolic interchange between the cells. They allow the transfer of small molecules and may enable slow calcium wave spreading, transfer of "death" or of "survival" signals. In the cardiomyocytes the most abundant isoform is Connexin 43 (Cx43). Alterations in Cx43 expression and distribution were observed in myocardium disease; i.e. in hypertrophic cardiomyopathy, heart failure and ischemia. Recent reports suggest the presence of Cx43 in the mitochondria as well, at least in the inner mitochondrial membrane, where it plays a central role in ischemic preconditioning. In this review, the current knowledge on the relationship between the remodeling of cardiac gap junctions and cardiac diseases are summarized
Methylguanidine, an uremic catabolyte, as possible responsible of altered immuneresponse.
No full text
Pro-apoptotic effect of methylguanidne on hydrogen peroxide-treated rat glioma cell line.
No full textL-Arginine and its metabolites in kidney and cardiovascular disease
No full textL-Arginine is a semi essential amino acid synthesised from glutamine, glutamate and proline via the intestinal-renal axis in humans and most mammals. L-Arginine degradation occurs via multiple pathways initiated by arginase, nitric-oxide synthase, Arg: glycine amidinotransferase, and Arg decarboxylase. These pathways produce nitric oxide, polyamines, proline, glutamate, creatine and agmatine with each having enormous biological importance. Several disease are associated to an L-arginine impaired levels and/or to its metabolites: in particular various L-arginine metabolites may participate in pathogenesis of kidney and cardiovascular disease. L-Arginine and its metabolites may constitute both a marker of pathology progression both the rationale for manipulating L-arginine metabolism as a strategy to ameliorate these disease. A large number of studies have been performed in experimental models of kidney disease with sometimes conflicting results, which underlie the complexity of Arg metabolism and our incomplete knowledge of all the mechanisms involved. Moreover several lines of evidence demonstrate the role of L-arg metabolites in cardiovascular disease and that L-arg administration role in reversing endothelial dysfunction, which is the leading cause of cardiovascular diseases, such as hypertension and atherosclerosis. This review will discuss the implication of the mains L-arginine metabolites and L-arginine-derived guanidine compounds in kidney and cardiovascular disease considering the more recent literature in the field
Severe acidosis affects the anti-inflammatory properties of N-acetylcysteine on lipopolysaccharide-activated macrophages
Full text linkCritical illness is exemplified by a state of profound disruption in physiological homeostatic mechanisms. Tissue acidosis is an hallmark of inflammation/ischemia and tumor processes and although it remains uncertain whether there is a true cause-effect relation between acidosis and adverse clinical outcomes it remains a powerful marker of poor prognosis in critically ill patients. Patients with severe sepsis and septic shock exhibit a complex metabolic pattern of acidosis at intensive care unit admission, caused predominantly by hyperchloremic acidosis, which was more pronounced in non survivors. Abnormalities in systemic acid-base balance may also induce significant alterations in the immune response. In this study we evaluated the effect of N-acetylcysteine (NAC), an important cellular antioxidant, during severe hyperchloremic acidosis, in vitro, in Lipopolysaccharide from E.coli (LPS)-treated J774A.1 murine/macrophage cell line. Our results show that NAC, in hyperchloremic acidosis conditions, reduces nitric oxide (NO) and reactive oxygen species (ROS) release and iNOS expression. Furthermore these effects are associated to alterations in J774A.1 macrophage cell cycle distribution but not to impairments of cell viability and apoptosis induction. Our data report a reduced inflammatory response exerted by NAC in condition of hyperchloremic acidosis indicating that the use of NAC during inflammation further impairs immune response associated to acidosis associated disease, as septic shock
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