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Article ; Online: Methods to Study NLR in Human Blood Cells.

Carta, Sonia / Gattorno, Marco / Rubartelli, Anna

Methods in molecular biology (Clifton, N.J.)

2023 Volume 2696, Page(s) 115–122

Abstract: Autoinflammatory diseases are a group of inherited and multifactorial disorders characterized by an over-activation of innate immune response. In most cases, the clinical manifestations are due to increased activity of the NLRP3 inflammasome resulting in ...

Abstract	Autoinflammatory diseases are a group of inherited and multifactorial disorders characterized by an over-activation of innate immune response. In most cases, the clinical manifestations are due to increased activity of the NLRP3 inflammasome resulting in increased IL-1β secretion. Investigating inflammatory cells from subjects affected by autoinflammatory diseases presents a number of technical difficulties related to the rarity of the diseases, to the young age of most patients, to the difficult modulation of gene expression in primary cells. However, since cell stress is involved in the pathophysiology of these diseases, the study of freshly drawn blood monocytes from patients affected by IL-1-mediated diseases strongly increases the chances that the observed phenomena is indeed pertinent to the pathogenesis of the disease and not influenced by the long-term cell culture conditions (e.g., the high O
MeSH term(s)	Humans ; NLR Family, Pyrin Domain-Containing 3 Protein/genetics ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Monocytes/metabolism ; Interleukin-1beta/metabolism ; Inflammasomes/metabolism ; Hereditary Autoinflammatory Diseases/metabolism
Chemical Substances	NLR Family, Pyrin Domain-Containing 3 Protein ; Interleukin-1beta ; Inflammasomes
Language	English
Publishing date	2023-08-14
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-3350-2_8
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Article ; Online: Unexpected chronic lymphocytic leukemia B cell activation by bisphosphonates.

Mazzarello, Andrea N / Gugiatti, Elena / Cossu, Vanessa / Bertola, Nadia / Bagnara, Davide / Carta, Sonia / Ravera, Silvia / Salvetti, Chiara / Ibatici, Adalberto / Ghiotto, Fabio / Colombo, Monica / Cutrona, Giovanna / Marini, Cecilia / Sambuceti, Gianmario / Fais, Franco / Bruno, Silvia

Cancer immunology, immunotherapy : CII

2024 Volume 73, Issue 2, Page(s) 27

Abstract: Chronic lymphocytic leukemia (CLL) is a disease of the elderly, often presenting comorbidities like osteoporosis and requiring, in a relevant proportion of cases, treatment with bisphosphonates (BPs). This class of drugs was shown in preclinical ... ...

Abstract	Chronic lymphocytic leukemia (CLL) is a disease of the elderly, often presenting comorbidities like osteoporosis and requiring, in a relevant proportion of cases, treatment with bisphosphonates (BPs). This class of drugs was shown in preclinical investigations to also possess anticancer properties. We started an in vitro study of the effects of BPs on CLL B cells activated by microenvironment-mimicking stimuli and observed that, depending on drug concentration, hormetic effects were induced on the leukemic cells. Higher doses induced cytotoxicity whereas at lower concentrations, more likely occurring in vivo, the drugs generated a protective effect from spontaneous and chemotherapy-induced apoptosis, and augmented CLL B cell activation/proliferation. This CLL-activation effect promoted by the BPs was associated with markers of poor CLL prognosis and required the presence of bystander stromal cells. Functional experiments suggested that this phenomenon involves the release of soluble factors and is increased by cellular contact between stroma and CLL B cells. Since CLL patients often present comorbidities such as osteoporosis and considering the diverse outcomes in both CLL disease progression and CLL response to treatment among patients, illustrating this phenomenon holds potential significance in driving additional investigations.
MeSH term(s)	Humans ; Aged ; Leukemia, Lymphocytic, Chronic, B-Cell/drug therapy ; Diphosphonates/pharmacology ; Diphosphonates/therapeutic use ; B-Lymphocytes ; Apoptosis ; Osteoporosis/drug therapy ; Tumor Microenvironment
Chemical Substances	Diphosphonates
Language	English
Publishing date	2024-01-27
Publishing country	Germany
Document type	Journal Article
ZDB-ID	195342-4
ISSN	1432-0851 ; 0340-7004
ISSN (online)	1432-0851
ISSN	0340-7004
DOI	10.1007/s00262-023-03588-z
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Article ; Online: 18

Sambuceti, Gianmario / Cossu, Vanessa / Bauckneht, Matteo / Morbelli, Silvia / Orengo, AnnaMaria / Carta, Sonia / Ravera, Silvia / Bruno, Silvia / Marini, Cecilia

European journal of nuclear medicine and molecular imaging

2021 Volume 48, Issue 5, Page(s) 1278–1286

MeSH term(s)	Biological Transport ; Fluorodeoxyglucose F18 ; Glucose ; Humans ; Positron-Emission Tomography ; Radiopharmaceuticals
Chemical Substances	Radiopharmaceuticals ; Fluorodeoxyglucose F18 (0Z5B2CJX4D) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2021-04-16
Publishing country	Germany
Document type	Editorial ; Research Support, Non-U.S. Gov't
ZDB-ID	8236-3
ISSN	1619-7089 ; 0340-6997 ; 1619-7070
ISSN (online)	1619-7089
ISSN	0340-6997 ; 1619-7070
DOI	10.1007/s00259-021-05368-2
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Article ; Online: Mandatory role of endoplasmic reticulum and its pentose phosphate shunt in the myocardial defense mechanisms against the redox stress induced by anthracyclines.

Sambuceti, Gianmario / Cossu, Vanessa / Vitale, Francesca / Bianconi, Eva / Carta, Sonia / Venturi, Consuelo / Chiesa, Sabrina / Lanfranchi, Francesco / Emionite, Laura / Carlone, Sebastiano / Sofia, Luca / D'Amico, Francesca / Di Raimondo, Tania / Chiola, Silvia / Orengo, Anna Maria / Morbelli, Silvia / Ameri, Pietro / Bauckneht, Matteo / Marini, Cecilia

Molecular and cellular biochemistry

2023

Abstract: Anthracyclines' cardiotoxicity involves an accelerated generation of reactive oxygen species. This oxidative damage has been found to accelerate the expression of hexose-6P-dehydrogenase (H6PD), that channels glucose-6-phosphate (G6P) through the pentose ...

Abstract	Anthracyclines' cardiotoxicity involves an accelerated generation of reactive oxygen species. This oxidative damage has been found to accelerate the expression of hexose-6P-dehydrogenase (H6PD), that channels glucose-6-phosphate (G6P) through the pentose phosphate pathway (PPP) confined within the endoplasmic/sarcoplasmic reticulum (SR). To verify the role of SR-PPP in the defense mechanisms activated by doxorubicin (DXR) in cardiomyocytes, we tested the effect of this drug in H6PD knockout mice (H6PD
Language	English
Publishing date	2023-12-12
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	184833-1
ISSN	1573-4919 ; 0300-8177
ISSN (online)	1573-4919
ISSN	0300-8177
DOI	10.1007/s11010-023-04903-z
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Article ; Online: Profound Modification of Fatty Acid Profile and Endocannabinoid-Related Mediators in PPARα Agonist Fenofibrate-Treated Mice

Elisabetta Murru / Anna Lisa Muntoni / Claudia Manca / Sonia Aroni / Marco Pistis / Sebastiano Banni / Gianfranca Carta

International Journal of Molecular Sciences, Vol 24, Iss 1, p

2022 Volume 709

Abstract: Fenofibrate (FBR), an oral medication used to treat dyslipidemia, is a ligand of the peroxisome proliferator-activated receptor α (PPARα), a nuclear receptor that regulates the expression of metabolic genes able to control lipid metabolism and food ... ...

Abstract	Fenofibrate (FBR), an oral medication used to treat dyslipidemia, is a ligand of the peroxisome proliferator-activated receptor α (PPARα), a nuclear receptor that regulates the expression of metabolic genes able to control lipid metabolism and food intake. PPARα natural ligands include fatty acids (FA) and FA derivatives such as palmitoylethanolamide (PEA) and oleoylethanolamide (OEA), known to have anti-inflammatory and anorexigenic activities, respectively. We investigated changes in the FA profile and FA derivatives by HPLC and LC-MS in male C57BL/6J mice fed a standard diet with or without 0.2% fenofibrate (0.2% FBR) for 21 days. Induction of PPARα by 0.2% FBR reduced weight gain, food intake, feed efficiency, and liver lipids and induced a profound change in FA metabolism mediated by parallel enhanced mitochondrial and peroxisomal β-oxidation. The former effects led to a steep reduction of essential FA, particularly 18:3n3, with a consequent decrease of the n3-highly unsaturated fatty acids (HUFA) score; the latter effect led to an increase of 16:1n7 and 18:1n9, suggesting enhanced hepatic de novo lipogenesis with increased levels of hepatic PEA and OEA, which may activate a positive feedback and further sustain reductions of body weight, hepatic lipids and feed efficiency.
Keywords	fenofibrate ; peroxisome proliferator-activated receptor α (PPARα) ; lipid metabolism ; n3-highly unsaturated fatty acid (HUFA) score ; endocannabinoids ; N -acylethanolamines ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	571
Language	English
Publishing date	2022-12-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article: Dysregulated IL-1β Secretion in Autoinflammatory Diseases: A Matter of Stress?

Carta, Sonia / Semino, Claudia / Sitia, Roberto / Rubartelli, Anna

Frontiers in immunology

2017 Volume 8, Page(s) 345

Abstract: Infectious and sterile inflammation is induced by activation of innate immune cells. Triggering of toll-like receptors by pathogen-associated molecular pattern or damage-associated molecular pattern (PAMP or DAMP) molecules generates reactive oxygen ... ...

Abstract	Infectious and sterile inflammation is induced by activation of innate immune cells. Triggering of toll-like receptors by pathogen-associated molecular pattern or damage-associated molecular pattern (PAMP or DAMP) molecules generates reactive oxygen species that in turn induce production and activation of pro-inflammatory cytokines such as IL-1β. Recent evidence indicates that cell stress due to common events, like starvation, enhanced metabolic demand, cold or heat, not only potentiates inflammation but may also directly trigger it in the absence of PAMPs or DAMPs. Stress-mediated inflammation is also a common feature of many hereditary disorders, due to the proteotoxic effects of mutant proteins. We propose that harmful mutant proteins can induce dysregulated IL-1β production and inflammation through different pathways depending on the cell type involved. When expressed in professional inflammatory cells, stress induced by the mutant protein activates in a cell-autonomous way the onset of inflammation and mediates its aberrant development, resulting in the explosive responses that hallmark autoinflammatory diseases. When expressed in non-immune cells, the mutant protein may cause the release of transcellular stress signals that trigger and propagate inflammation.
Language	English
Publishing date	2017
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2606827-8
ISSN	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2017.00345
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Article ; Online: Therapeutic efficacy of proton transport inhibitors alone or in combination with cisplatin in triple negative and hormone sensitive breast cancer models.

Balza, Enrica / Carlone, Sebastiano / Carta, Sonia / Piccioli, Patrizia / Cossu, Vanessa / Marini, Cecilia / Sambuceti, Gianmario / Rubartelli, Anna / Castellani, Patrizia

Cancer medicine

2021 Volume 11, Issue 1, Page(s) 183–193

Abstract: Triple negative breast cancers (TNBCs) are very aggressive and have a poor prognosis due to lack of efficacious therapies. The only effective treatment is chemotherapy that however is frequently hindered by the occurrence of drug resistance. We ... ...

Abstract	Triple negative breast cancers (TNBCs) are very aggressive and have a poor prognosis due to lack of efficacious therapies. The only effective treatment is chemotherapy that however is frequently hindered by the occurrence of drug resistance. We approached this problem in vitro and in vivo on a triple negative and a hormone sensitive breast cancer cell lines: 4T1 and TS/A. A main defense mechanism of tumors is the extrusion of intracellular protons derived from the metabolic shift to glycolysis, and necessary to maintain an intracellular pH compatible with life. The resulting acidic extracellular milieu bursts the malignant behavior of tumors and impairs chemotherapy. Therefore, we investigated the efficacy of combined therapies that associate cisplatin (Cis) with proton exchanger inhibitors, such as esomeprazole (ESO) and 5-(N-ethyl-N-isopropyl)amiloride (EIPA). Our results demonstrate that in the 4T1 triple negative model the combined therapy Cis plus EIPA is significantly more effective than the other treatments. Instead, in the TS/A tumor the best therapeutic result is obtained with ESO alone. Remarkably, in both 4T1 and TS/A tumors these treatments correlate with increase of CD8
MeSH term(s)	Amiloride/analogs & derivatives ; Amiloride/therapeutic use ; Animals ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; CD8-Positive T-Lymphocytes/metabolism ; Cell Line, Tumor ; Cell Proliferation ; Cisplatin/therapeutic use ; Esomeprazole/therapeutic use ; Female ; Humans ; Hydrogen-Ion Concentration ; Mice, Inbred BALB C ; Proton Pump Inhibitors/therapeutic use ; Sodium-Hydrogen Exchanger 1/metabolism ; Triple Negative Breast Neoplasms/drug therapy ; Triple Negative Breast Neoplasms/metabolism ; Tumor-Associated Macrophages/metabolism ; Vacuolar Proton-Translocating ATPases/metabolism ; Mice
Chemical Substances	Proton Pump Inhibitors ; Sodium-Hydrogen Exchanger 1 ; Amiloride (7DZO8EB0Z3) ; Vacuolar Proton-Translocating ATPases (EC 3.6.1.-) ; Esomeprazole (N3PA6559FT) ; Cisplatin (Q20Q21Q62J) ; ethylisopropylamiloride (VW50CE070T)
Language	English
Publishing date	2021-11-18
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2659751-2
ISSN	2045-7634 ; 2045-7634
ISSN (online)	2045-7634
ISSN	2045-7634
DOI	10.1002/cam4.4371
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Article ; Online: Progressive waves of IL-1β release by primary human monocytes via sequential activation of vesicular and gasdermin D-mediated secretory pathways.

Semino, Claudia / Carta, Sonia / Gattorno, Marco / Sitia, Roberto / Rubartelli, Anna

Cell death & disease

2018 Volume 9, Issue 11, Page(s) 1088

Abstract: IL-1β is an essential cytokine, but its release needs to be strictly controlled to avoid severe inflammatory manifestations. Lacking a signal sequence, IL-1β does not follow the endoplasmic reticulum-Golgi route. Several pathways have been proposed to ... ...

Abstract	IL-1β is an essential cytokine, but its release needs to be strictly controlled to avoid severe inflammatory manifestations. Lacking a signal sequence, IL-1β does not follow the endoplasmic reticulum-Golgi route. Several pathways have been proposed to mediate its release. One involves the translocation of pro-IL-1β into intracellular vesicles of lysosomal origin that eventually fuse with the plasma membrane. Another exploits pores formed on the plasma membrane upon proteolytic cleavage of gasdermin D (GSDMD). Here we investigated how primary monocytes-the main source of IL-1β in humans-control IL-1β release in response to pro-inflammatory stimuli of increasing intensity and found that two different routes are induced depending on the strength of activation. Triggering of Toll-like receptor 4 (TLR4) by LPS induces slow IL-1β release through LAMP2A
MeSH term(s)	Adolescent ; Adult ; Apoptosis ; Cells, Cultured ; Child ; Child, Preschool ; Cryopyrin-Associated Periodic Syndromes/blood ; Cryopyrin-Associated Periodic Syndromes/metabolism ; Cryopyrin-Associated Periodic Syndromes/pathology ; Female ; Humans ; Interleukin-1beta/metabolism ; Intracellular Signaling Peptides and Proteins/metabolism ; Lipopolysaccharides/pharmacology ; Lysosomal-Associated Membrane Protein 2/metabolism ; Male ; Monocytes/drug effects ; Monocytes/metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein/genetics ; Phosphate-Binding Proteins/metabolism ; Pyroptosis ; Reactive Oxygen Species/metabolism ; Secretory Pathway ; Toll-Like Receptors/metabolism ; Transport Vesicles/metabolism ; Young Adult ; Zymosan/pharmacology
Chemical Substances	GSDMD protein, human ; Interleukin-1beta ; Intracellular Signaling Peptides and Proteins ; LAMP2 protein, human ; Lipopolysaccharides ; Lysosomal-Associated Membrane Protein 2 ; NLR Family, Pyrin Domain-Containing 3 Protein ; NLRP3 protein, human ; Phosphate-Binding Proteins ; Reactive Oxygen Species ; Toll-Like Receptors ; Zymosan (9010-72-4)
Language	English
Publishing date	2018-10-23
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-018-1121-9
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Article ; Online: Gene's expression underpinning the divergent predictive value of [18F]F-fluorodeoxyglucose and prostate-specific membrane antigen positron emission tomography in primary prostate cancer: a bioinformatic and experimental study.

Journal of translational medicine

2023 Volume 21, Issue 1, Page(s) 3

Abstract: Background: Positron Emission Tomography (PET) imaging with Prostate-Specific Membrane Antigen (PSMA) and Fluorodeoxyglucose (FDG) represent promising biomarkers for risk-stratification of Prostate Cancer (PCa). We verified whether the expression of ... ...

Abstract	Background: Positron Emission Tomography (PET) imaging with Prostate-Specific Membrane Antigen (PSMA) and Fluorodeoxyglucose (FDG) represent promising biomarkers for risk-stratification of Prostate Cancer (PCa). We verified whether the expression of genes encoding for PSMA and enzymes regulating FDG cellular uptake are independent and additive prognosticators in PCa. Methods: mRNA expression of genes involved in glucose metabolism and PSMA regulation obtained from primary PCa specimens were retrieved from open-source databases and analyzed using an integrative bioinformatics approach. Machine Learning (ML) techniques were used to create predictive Progression-Free Survival (PFS) models. Cellular models of primary PCa with different aggressiveness were used to compare [18F]F-PSMA-1007 and [18F]F-FDG uptake kinetics in vitro. Confocal microscopy, immunofluorescence staining, and quantification analyses were performed to assess the intracellular and cellular membrane PSMA expression. Results: ML analyses identified a predictive functional network involving four glucose metabolism-related genes: ALDOB, CTH, PARP2, and SLC2A4. By contrast, FOLH1 expression (encoding for PSMA) did not provide any additive predictive value to the model. At a cellular level, the increase in proliferation rate and migratory potential by primary PCa cells was associated with enhanced FDG uptake and decreased PSMA retention (paralleled by the preferential intracellular localization). Conclusions: The overexpression of a functional network involving four glucose metabolism-related genes identifies a higher risk of disease progression since the earliest phases of PCa, in agreement with the acknowledged prognostic value of FDG PET imaging. By contrast, the prognostic value of PSMA PET imaging is independent of the expression of its encoding gene FOLH1. Instead, it is influenced by the protein docking to the cell membrane, regulating its accessibility to tracer binding.
MeSH term(s)	Humans ; Male ; Fluorodeoxyglucose F18 ; Glucose/metabolism ; Positron-Emission Tomography/methods ; Prostate/diagnostic imaging ; Prostate/metabolism ; Prostatic Neoplasms/diagnostic imaging ; Prostatic Neoplasms/genetics ; Prostatic Neoplasms/metabolism ; Machine Learning
Chemical Substances	Fluorodeoxyglucose F18 (0Z5B2CJX4D) ; Glucose (IY9XDZ35W2) ; FOLH1 protein, human (EC 3.4.17.21)
Language	English
Publishing date	2023-01-04
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2118570-0
ISSN	1479-5876 ; 1479-5876
ISSN (online)	1479-5876
ISSN	1479-5876
DOI	10.1186/s12967-022-03846-1
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Article ; Online: NLR in Human Diseases: Role and Laboratory Findings.

Carta, Sonia / Gattorno, Marco / Rubartelli, Anna

Methods in molecular biology (Clifton, N.J.)

2016 Volume 1417, Page(s) 247–254

Abstract: Autoinflammatory diseases are a group of inherited and multifactorial disorders characterized by an overactivation of innate immune response. In most cases, the clinical manifestations are due to increased activity of the NLRP3 inflammasome resulting in ... ...

Abstract	Autoinflammatory diseases are a group of inherited and multifactorial disorders characterized by an overactivation of innate immune response. In most cases, the clinical manifestations are due to increased activity of the NLRP3 inflammasome resulting in increased IL-1β secretion. Investigating inflammatory cells from subjects affected by autoinflammatory diseases presents a number of technical difficulties related to the rarity of the diseases, to the young age of most patients, and to the difficult modulation of gene expression in primary cells. However, since cell stress is involved in the pathophysiology of these diseases, the study of freshly drawn blood monocytes from patients affected by IL-1-mediated diseases strongly increases the chances that the observed phenomena is indeed pertinent to the pathogenesis of the disease and not influenced by the long-term cell culture conditions (e.g., the high O2 tension) or gene transfection in continuous cell lines that may lead to artifacts.
Language	English
Publishing date	2016
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-4939-3566-6_18
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