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3 results on '"Rosita, Stanzione"'

1. An interplay between UCP2 and ROS protects cells from high-salt-induced injury through autophagy stimulation

Author

Maurizio Forte, Franca Bianchi, Maria Cotugno, Simona Marchitti, Rosita Stanzione, Vittorio Maglione, Sebastiano Sciarretta, Valentina Valenti, Roberto Carnevale, Francesco Versaci, Giacomo Frati, Massimo Volpe, and Speranza Rubattu

Subjects
Cytology, QH573-671
Abstract

Abstract The mitochondrial uncoupling protein 2 (UCP2) plays a protective function in the vascular disease of both animal models and humans. UCP2 downregulation upon high-salt feeding favors vascular dysfunction in knock-out mice, and accelerates cerebrovascular and renal damage in the stroke-prone spontaneously hypertensive rat. Overexpression of UCP2 counteracts the negative effects of high-salt feeding in both animal models. We tested in vitro the ability of UCP2 to stimulate autophagy and mitophagy as a mechanism mediating its protective effects upon high-salt exposure in endothelial and renal tubular cells. UCP2 silencing reduced autophagy and mitophagy, whereas the opposite was true upon UCP2 overexpression. High-salt exposure increased level of reactive oxygen species (ROS), UCP2, autophagy and autophagic flux in both endothelial and renal tubular cells. In contrast, high-salt was unable to induce autophagy and autophagic flux in UCP2-silenced cells, concomitantly with excessive ROS accumulation. The addition of an autophagy inducer, Tat-Beclin 1, rescued the viability of UCP2-silenced cells even when exposed to high-salt. In summary, UCP2 mediated the interaction between high-salt-induced oxidative stress and autophagy to preserve viability of both endothelial and renal tubular cells. In the presence of excessive ROS accumulation (achieved upon UCP2 silencing and high-salt exposure of silenced cells) autophagy was turned off. In this condition, an exogenous autophagy inducer rescued the cellular damage induced by excess ROS level. Our data confirm the protective role of UCP2 toward high-salt-induced vascular and renal injury, and they underscore the role of autophagy/mitophagy as a mechanism counteracting the high-salt-induced oxidative stress damage.

Published
2021
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2. Natriuretic peptides: An update on bioactivity, potential therapeutic use, and implication in cardiovascular diseases

Author

Massimo Volpe, Speranza Rubattu, Sebastiano Sciarretta, Valentina Valenti, and Rosita Stanzione

Subjects
medicine.medical_specialty, medicine.drug_class, Blood Pressure, Context (language use), Bioinformatics, Ventricular Dysfunction, Left, Atrial natriuretic peptide, Risk Factors, Internal medicine, Natriuretic Peptide, Brain, Internal Medicine, medicine, Natriuretic peptide, Humans, Natriuretic Peptides, Ventricular remodeling, Inflammation, Ventricular Remodeling, business.industry, Myocardium, Natriuretic Peptide, C-Type, Lipid Metabolism, medicine.disease, Brain natriuretic peptide, Fibrosis, Blood pressure, Cardiovascular Diseases, Heart failure, cardiovascular system, Cardiology, Blood Vessels, Insulin Resistance, Metabolic syndrome, business, Atrial Natriuretic Factor, Biomarkers
Abstract

The natriuretic peptide system includes three known peptides: atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP). They contribute to the regulation of cardiovascular homeostasis through diuretic, natriuretic, and vasodilatory properties. Among them, ANP has received particular attention because of its effects on blood pressure regulation and cardiac function. Although the potential for its therapeutic application in the treatment of hypertension and heart failure has been evaluated in several experimental and clinical investigations, no pharmacological approach directly targeted at modulation of ANP levels has ever reached the stage of being incorporated into clinical practice. Recently, ANP has also received attention as being a possible cardiovascular risk factor, particularly in the context of hypertension, stroke, obesity, and metabolic syndrome. Abnormalities in either peptide levels or peptide structure are thought to underlie its implied role in mediating cardiovascular diseases. Meanwhile, BNP has emerged as a relevant marker of left ventricular (LV) dysfunction and as a useful predictor of future outcome in patients with heart failure. This review deals with the major relevant findings related to the cardiovascular and metabolic effects of natriuretic peptides, to their potential therapeutic use, and to their role in mediating cardiovascular diseases.

Published
2008

3. C2238/αANP modulates apolipoprotein E through Egr-1/miR199a in vascular smooth muscle cells in vitro

Author

Sebastiano Sciarretta, Simona Marchitti, Giacomo Frati, Franca Bianchi, Massimo Volpe, M Cotugno, Stefania Scarpino, Rosita Stanzione, S Di Castro, and Speranza Rubattu

Subjects
Apolipoprotein E, Cancer Research, medicine.medical_specialty, Umbilical Veins, Vascular smooth muscle, Cell Survival, Immunology, Myocytes, Smooth Muscle, Inflammation, Apoptosis, Biology, Real-Time Polymerase Chain Reaction, Models, Biological, Muscle, Smooth, Vascular, Cellular and Molecular Neuroscience, Necrosis, Apolipoproteins E, Downregulation and upregulation, Internal medicine, medicine, Myocyte, Humans, RNA, Messenger, atrial natriuretic factor alpha, Receptor, apolipoprotein E, Early Growth Response Protein 1, Gene knockdown, Wild type, Cell Biology, Atherosclerosis, Coronary Vessels, natriuretic peptide receptor C, Up-Regulation, MicroRNAs, Endocrinology, Mutation, early growth response factor 1, heat shock protein 40, Original Article, medicine.symptom, Reactive Oxygen Species, Receptors, Atrial Natriuretic Factor, Atrial Natriuretic Factor, Biomarkers
Abstract

Subjects carrying the T2238C ANP gene variant have a higher risk to suffer a stroke or myocardial infarction. The mechanisms through which T2238C/αANP exerts detrimental vascular effects need to be fully clarified. In the present work we aimed at exploring the impact of C2238/αANP (mutant form) on atherosclerosis-related pathways. As a first step, an atherosclerosis gene expression macroarray analysis was performed in vascular smooth muscle cells (VSMCs) exposed to either T2238/αANP (wild type) or C2238/αANP. The major finding was that apolipoprotein E (ApoE) gene expression was significantly downregulated by C2238/αANP and it was upregulated by T2238/αANP. We subsequently found that C2238/αANP induces ApoE downregulation through type C natriuretic peptide receptor (NPR-C)-dependent mechanisms involving the upregulation of miR199a-3p and miR199a-5p and the downregulation of DNAJA4. In fact, NPR-C knockdown rescued ApoE level. Upregulation of miR199a by NPR-C was mediated by a reactive oxygen species-dependent increase of the early growth response protein-1 (Egr-1) transcription factor. In fact, Egr-1 knockdown abolished the impact of C2238/αANP on ApoE and miR199a. Of note, downregulation of ApoE by C2238/αANP was associated with a significant increase in inflammation, apoptosis and necrosis that was completely rescued by the exogenous administration of recombinant ApoE. In conclusion, our study dissected a novel mechanism of vascular damage exerted by C2238/αANP that is mediated by ApoE downregulation. We provide the first demonstration that C2238/αANP downregulates ApoE in VSMCs through NPR-C-dependent activation of Egr-1 and the consequent upregulation of miR199a. Restoring ApoE levels could represent a potential therapeutic strategy to counteract the harmful effects of C2238/αANP.

Published
2015

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