Search results for: Mariapaola Nitti

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HO‐1 downregulation favors BRAF^V600 melanoma cell death induced by Vemurafenib/PLX4032 and increases NK recognition

Anna L. Furfaro, Selene Ottonello, Giulia Loi, Irene Cossu, more

International Journal of Cancer > 146 > 7 > 1950 - 1962

Heme oxygenase 1 (HO‐1) plays a pivotal role in preventing cell damage. Indeed, through the antioxidant, antiapoptotic and anti‐inflammatory properties of its metabolic products, it favors cell adaptation against different stressors. However, HO‐1 induction has also been related to the gain of resistance to therapy in different types of cancers and its involvement in cancer immune‐escape has been...

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HO-1 down-regulation increases the efficacy of BRAFV600E inhibition-based therapy in primary melanoma cells

Anna Lisa Furfaro, Gabriella Pietra, Irene Cossu, Umberto M. Marinari, more

Free Radical Biology and Medicine > 2017 > 108 > S1 > S64

Heme oxygenase 1 (HO-1) plays a key role in maintaining cell redox balance. Under stress conditions, HO-1 is up-regulated and generates bilirubin, ferritin and carbon monoxide, with antioxidant, antiapoptotic and anti-inflammatory properties [Jozkowicz et al., 2007]. HO-1 induction favors cancer progression [Furfaro et al., 2016] and its involvement in tumor resistance to therapy [Was et al., 2006]...

article

Differentiation modifies Bach1 dependent regulation of HO-1 expression and increases sensitivity to oxidative stress in neuroblastoma cells

Sabrina Piras, Lorenzo Brondolo, Anna Lisa Furfaro, Mario Passalacqua, more

Free Radical Biology and Medicine > 2017 > 108 > S1 > S80

Neuronal adaptation to oxidative stress is crucial to prevent degenerative diseases. The role of the Nrf2/HO-1 system in cell response to hydrogen peroxide (H₂O₂) has been investigated using SH-SY5Y neuroblastoma cells as undifferentiated or after differentiation with all-trans retinoic acid (ATRA). We showed that undifferentiated cells resisted to oxidative stimulus and up-regulated HO-1 which was...

article

HO-1 Down-Regulation Increases the Efficacy of BRAFV600E Inhibition-Based Therapy in Primary Melanoma Cells

Anna Lisa Furfaro, Gabriella Pietra, Umberto Maria Marinari, Lorenzo Moretta, more

Free Radical Biology and Medicine > 2016 > 100 > S > S122

The inducible enzyme heme oxygenase 1 (HO-1) plays a crucial role in maintaining redox balance. Under stress conditions, HO-1 is up-regulated leading to the generation of bilirubin, ferritin and carbon monoxide, with antioxidant, antiapoptotic and anti-inflammatory properties [1]. The induction of HO-1 is involved in the gain of resistance to oxidation-based therapies and favors cancer progression...

article

Neuroblastoma Cell Response to Oxidative Stress Is Impaired by Retinoic Acid-Induced Differentiation: Role of HO-1

Mariapaola Nitti, Sabrina Piras, Anna Lisa Furfaro, Lorenzo Brondolo, more

Free Radical Biology and Medicine > 2016 > 100 > S > S106-S107

The modulation of redox balance is able to drive different cell functions, from differentiation to proliferation. In a previous work, we showed that all-trans retinoic acid (ATRA) induced differentiation of SH-SY5Y neuroblastoma (NB) cells through the generation of reactive oxygen species (ROS) [Nitti et al Cell Signal 2010]. However, ATRA-differentiated NB cells resulted more sensitive to the further...

article

ATRA-induced neuronal differentiation reduces cell ability to adapt to oxidative stress: role of Nrf2 and HO-1

Sabrina Piras, Anna Lisa Furfaro, Cinzia Domenicotti, Nicola Traverso, more

Free Radical Biology and Medicine > 2016 > 96 > S1 > S49

article

Heme oxygenase-1-derived bilirubin protects endothelial cells against high glucose-induced damage

Meihua He, Mariapaola Nitti, Sabrina Piras, Anna Lisa Furfaro, more

Free Radical Biology and Medicine > 2015 > 89 > C > 91-98

Hyperglycemia and diabetes are associated with endothelial cell dysfunction arising from enhanced oxidative injury, leading to the progression of diabetic vascular pathologies. The redox-sensitive transcription factor nuclear factor-E2-related factor 2 (Nrf2) is a master regulator of antioxidant genes, such as heme oxygenase-1 (HO-1), involved in cellular defenses against oxidative stress. We have...

article

Monomeric Aβ1–42 and RAGE: key players in neuronal differentiation

Sabrina Piras, Anna L. Furfaro, Alessandra Piccini, Mario Passalacqua, more

Neurobiology of Aging > 2014 > 35 > 6 > 1301-1308

The aggregation of amyloid-β (Aβ) peptides plays a crucial role in the onset and progression of Alzheimer's disease. Monomeric form of Aβ, indeed, could exert a physiological role. Considering the anti-oligomerization property of all-trans retinoic acid (ATRA), the involvement of monomeric Aβ1–42 in ATRA-induced neuronal differentiation has been investigated. Four-day ATRA treatment increases β-secretase...

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HO-1 up-regulation: A key point in high-risk neuroblastoma resistance to bortezomib

Anna Lisa Furfaro, Sabrina Piras, Mario Passalacqua, Cinzia Domenicotti, more

BBA - Molecular Basis of Disease > 2014 > 1842 > 4 > 613-622

High-risk neuroblastoma (NB) is characterized by the development of chemoresistance, and bortezomib (BTZ), a selective inhibitor of proteasome, has been proposed in order to overcome drug resistance. Considering the involvement of the nuclear factor-erythroid-derived 2-like 2 (Nrf2) and heme oxygenase-1 (HO-1) in the antioxidant and detoxifying ability of cancer cells, in this study we have investigated...

article

Short exposure of albumin to high concentrations of malondialdehyde does not mimic physiological conditions

Susanna Millanta, Anna Lisa Furfaro, Paolo Carlier, Bruno Tasso, more

Experimental and Molecular Pathology > 2013 > 94 > 1 > 270-276

Malondialdehyde (MDA), a major lipid peroxidation product, spontaneously binds to, and modifies proteins. In vivo, proteins are physiologically exposed to micromolar MDA concentrations for long periods. In order to mimic this process in vitro, protein modification is often performed by short exposure to millimolar MDA concentrations, also in order to generate antigenic structures for antibody production...

article

Resistance of neuroblastoma GI-ME-N cell line to glutathione depletion involves Nrf2 and heme oxygenase-1

Anna Lisa Furfaro, José Raúl Zumba Macay, Barbara Marengo, Mariapaola Nitti, more

Free Radical Biology and Medicine > 2012 > 52 > 2 > 488-496

Cancer cell survival is known to be related to the ability to counteract oxidative stress, and glutathione (GSH) depletion has been proposed as a mechanism to sensitize cells to anticancer therapy. However, we observed that GI-ME-N cells, a neuroblastoma cell line without MYCN amplification, are able to survive even if GSH-depleted by l-buthionine-(S,R)-sulfoximine (BSO). Here, we show that in GI-ME-N...

article

PKC delta and NADPH oxidase in retinoic acid-induced neuroblastoma cell differentiation

Mariapaola Nitti, Anna Lisa Furfaro, Claudia Cevasco, Nicola Traverso, more

Cellular Signalling > 2010 > 22 > 5 > 828-835

The role of reactive oxygen species (ROS) in the regulation of signal transduction processes has been well established in many cell types and recently the fine tuning of redox signalling in neurons received increasing attention. With regard to this, the involvement of NADPH oxidase (NOX) in neuronal pathophysiology has been proposed but deserves more investigation. In the present study, we used SH-SY5Y...

article

PKC signaling in oxidative hepatic damage

Mariapaola Nitti, Maria A. Pronzato, Umberto M. Marinari, Cinzia Domenicotti

Molecular Aspects of Medicine > 2008 > 29 > 1-2 > 36-42

Protein kinase C (PKC) is a family of isoenzymes differently involved in cell response to injury and many studies describe their role as “stress sensors”. Oxidative stress is strictly involved in the pathogenesis of chronic liver diseases including alcohol- or drug-induced hepatotoxicity, iron overload, hepatitis and hepatocarcinoma development, but molecular mechanisms are not really defined. A crucial...

article

PKC delta and NADPH oxidase in AGE-induced neuronal death

Mariapaola Nitti, Anna L. Furfaro, Nicola Traverso, Patrizio Odetti, more

Neuroscience Letters > 2007 > 416 > 3 > 261-265

Advanced glycation end product (AGE) accumulation in brain is believed to contribute to neuronal death in several neurodegenerative diseases. Neurons exposed to AGEs undergo oxidative stress, but the molecular mechanisms able to induce ROS generation and cell death are not yet clear. In this work, we exposed SH-SY5Y neuroblastoma cells to glycated albumin, as a model of AGE-modified protein, and we...

article

Heme oxygenase 1 expression in rat liver during ageing and ethanol intoxication

Stefania Patriarca, Anna Lisa Furfaro, Luana Cosso, Elena Pesce Maineri, more

Biogerontology > 2007 > 8 > 3 > 365-372

Heme oxygenase 1 (HO-1) expression is recognized as a marker of cellular response to oxidative stress; since ageing is believed to be related to oxidative “wear and tear”, HO-1 may represent a candidate biomarker of ageing. In our study, the hepatic expression of HO-1 mRNA, evaluated by RT-PCR in 2.5–24 month-old rats, was higher at 6 months than at 2.5 months of age, but thereafter increased no further:...

article

Central role of PKCδ in glycoxidation-dependent apoptosis of human neurons

Mariapaola Nitti, Cristina d'Abramo, Nicola Traverso, Daniela Verzola, more

Free Radical Biology and Medicine > 2005 > 38 > 7 > 846-856

Accumulation of advanced glycation end products (AGEs) induces alterations in the intracellular redox balance, leading cells to functional injury. Current literature reports that intracellular signaling triggered by the interaction of AGEs with their specific receptors RAGEs depends on the cell type and the state of activation/stress. In this work, NT2 human neurons were exposed for 48 h to glycated...

article

A novel role of protein kinase C-δ in cell signaling triggered by glutathione depletion

Cinzia Domenicotti, Barbara Marengo, Mariapaola Nitti, Daniela Verzola, more

Biochemical Pharmacology > 2003 > 66 > 8 > 1521-1526

Current evidence demonstrates that protein kinase C (PKC) belongs to a group of cell-signaling molecules that are sensitive targets for redox modifications and functional alterations that mediate oxidant-induced cellular responses. Our studies have demonstrated that diminished intracellular GSH was associated to inactivation of classic isoforms and increased activity of novel PKCs, and triggered molecular...

article

Role of PKC-dependent pathways in HNE-induced cell protein transport and secretion

Umberto Maria Marinari, Mariapaola Nitti, Maria Adelaide Pronzato, Cinzia Domenicotti

Molecular Aspects of Medicine > 2003 > 24 > 4-5 > 205-211

The β isoforms of protein Kinase C (PKC) are closely involved in the regulation of cell protein transport and secretion. We have shown in different cellular types that treatment with HNE in a concentration range detectable in many pathophysiological conditions is able to induce selective activation of βPKCs through direct interaction between the aldehyde and these isoenzymes. In isolated rat hepatocytes...

article

Glutathione depletion induces apoptosis of rat hepatocytes through activation of protein kinase C novel isoforms and dependent increase in AP-1 nuclear binding

Cinzia Domenicotti, Dimitri Paola, Antonella Vitali, Mariapaola Nitti, more

Free Radical Biology and Medicine > 2000 > 29 > 12 > 1280-1290

Treatment of isolated rat hepatocytes with the glutathione depleting agents L-buthionine-S,R-sulfoximine or diethylmaleate reproduced various cellular conditions of glutathione depletion, from moderate to severe, similar to those occurring in a wide spectrum of human liver diseases. To evaluate molecular changes and possible cellular dysfunction and damage consequent to a pathophysiologic level of...

article

Oxidative Stress Induces Increase in Intracellular Amyloid β-Protein Production and Selective Activation of βI and βII PKCs in NT2 Cells - Volume 268, Number 2 (2000), pages 642-646 (doi:10.1006/bbrc.2000.2164)

Dimitri Paola, Cinzia Domenicotti, Mariapaola Nitti, Antonella Vitali, more

Biochemical and Biophysical Research Communications > 2000 > 272 > 1 > 309

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Search results for: Mariapaola Nitti

HO‐1 downregulation favors BRAF^V600 melanoma cell death induced by Vemurafenib/PLX4032 and increases NK recognition

HO-1 down-regulation increases the efficacy of BRAFV600E inhibition-based therapy in primary melanoma cells

Differentiation modifies Bach1 dependent regulation of HO-1 expression and increases sensitivity to oxidative stress in neuroblastoma cells

HO-1 Down-Regulation Increases the Efficacy of BRAFV600E Inhibition-Based Therapy in Primary Melanoma Cells

Neuroblastoma Cell Response to Oxidative Stress Is Impaired by Retinoic Acid-Induced Differentiation: Role of HO-1

ATRA-induced neuronal differentiation reduces cell ability to adapt to oxidative stress: role of Nrf2 and HO-1

Heme oxygenase-1-derived bilirubin protects endothelial cells against high glucose-induced damage

Monomeric Aβ1–42 and RAGE: key players in neuronal differentiation

HO-1 up-regulation: A key point in high-risk neuroblastoma resistance to bortezomib

Short exposure of albumin to high concentrations of malondialdehyde does not mimic physiological conditions

Resistance of neuroblastoma GI-ME-N cell line to glutathione depletion involves Nrf2 and heme oxygenase-1

PKC delta and NADPH oxidase in retinoic acid-induced neuroblastoma cell differentiation

PKC signaling in oxidative hepatic damage

PKC delta and NADPH oxidase in AGE-induced neuronal death

Heme oxygenase 1 expression in rat liver during ageing and ethanol intoxication

Central role of PKCδ in glycoxidation-dependent apoptosis of human neurons

A novel role of protein kinase C-δ in cell signaling triggered by glutathione depletion

Role of PKC-dependent pathways in HNE-induced cell protein transport and secretion

Glutathione depletion induces apoptosis of rat hepatocytes through activation of protein kinase C novel isoforms and dependent increase in AP-1 nuclear binding

Oxidative Stress Induces Increase in Intracellular Amyloid β-Protein Production and Selective Activation of βI and βII PKCs in NT2 Cells - Volume 268, Number 2 (2000), pages 642-646 (doi:10.1006/bbrc.2000.2164)

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