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Article ; Online: NLRP3 and Infections: β-Amyloid in Inflammasome beyond Neurodegeneration.

Sita, Giulia / Graziosi, Agnese / Hrelia, Patrizia / Morroni, Fabiana

International journal of molecular sciences

2021 Volume 22, Issue 13

Abstract: Amyloid beta (Aβ)-induced abnormal neuroinflammation is recognized as a major pathological feature of Alzheimer's disease (AD), which results in memory impairment. Research exploring low-grade systemic inflammation and its impact on the development and ... ...

Abstract	Amyloid beta (Aβ)-induced abnormal neuroinflammation is recognized as a major pathological feature of Alzheimer's disease (AD), which results in memory impairment. Research exploring low-grade systemic inflammation and its impact on the development and progression of neurodegenerative disease has increased. A particular research focus has been whether systemic inflammation arises only as a secondary effect of disease, or it is also a cause of pathology. The inflammasomes, and more specifically the NLRP3 inflammasome, are crucial components of the innate immune system and are usually activated in response to infection or tissue damage. Although inflammasome activation plays critical roles against various pathogens in host defense, overactivation of inflammasome contributes to the pathogenesis of inflammatory diseases, including acute central nervous system (CNS) injuries and chronic neurodegenerative diseases, such as AD. This review summarizes the current literature on the role of the NLRP3 inflammasome in the pathogenesis of AD, and its involvement in infections, particularly SARS-CoV-2. NLRP3 might represent the crossroad between the hypothesized neurodegeneration and the primary COVID-19 infection.
MeSH term(s)	Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Amyloid beta-Peptides/metabolism ; Animals ; Coronavirus/pathogenicity ; Humans ; Immunity, Innate ; Inflammasomes/metabolism ; Microglia/metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Virus Diseases/immunology ; Virus Diseases/pathology
Chemical Substances	Amyloid beta-Peptides ; Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein
Language	English
Publishing date	2021-06-29
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms22136984
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Article ; Online: Sulforaphane Causes Cell Cycle Arrest and Apoptosis in Human Glioblastoma U87MG and U373MG Cell Lines under Hypoxic Conditions.

Sita, Giulia / Graziosi, Agnese / Hrelia, Patrizia / Morroni, Fabiana

International journal of molecular sciences

2021 Volume 22, Issue 20

Abstract: Glioblastoma multiforme (GBM) is the most prevalent and aggressive primary brain tumor. The median survival rate from diagnosis ranges from 15 to 17 months because the tumor is resistant to most therapeutic strategies. GBM exhibits microvascular ... ...

Abstract	Glioblastoma multiforme (GBM) is the most prevalent and aggressive primary brain tumor. The median survival rate from diagnosis ranges from 15 to 17 months because the tumor is resistant to most therapeutic strategies. GBM exhibits microvascular hyperplasia and pronounced necrosis triggered by hypoxia. Sulforaphane (SFN), an isothiocyanate derived from cruciferous vegetables, has already demonstrated the ability to inhibit cell proliferation, by provoking cell cycle arrest, and leading to apoptosis in many cell lines. In this study, we investigated the antineoplastic effects of SFN [20-80 μM for 48 h] in GBM cells under normoxic and hypoxic conditions. Cell viability assays, flow cytometry, and Western blot results revealed that SFN could induce apoptosis of GBM cells in a dose-dependent manner, under both conditions. In particular, SFN significantly induced caspase 3/7 activation and DNA fragmentation. Moreover, our results demonstrated that SFN suppressed GBM cells proliferation by arresting the cell cycle at the S-phase, also under hypoxic condition, and that these effects may be due in part to its ability to induce oxidative stress by reducing glutathione levels and to increase the phosphorylation of extracellular signal-regulated kinases (ERKs). Overall, we hypothesized that SFN treatment might serve as a potential therapeutic strategy, alone or in combination, against GBM.
MeSH term(s)	Antineoplastic Agents, Phytogenic/administration & dosage ; Antineoplastic Agents, Phytogenic/pharmacology ; Apoptosis/drug effects ; Brain Neoplasms/drug therapy ; Brain Neoplasms/metabolism ; Brain Neoplasms/pathology ; Cell Cycle Checkpoints/drug effects ; Cell Line, Tumor ; Cell Movement/drug effects ; Cell Survival/drug effects ; Dose-Response Relationship, Drug ; Glioblastoma/drug therapy ; Glioblastoma/metabolism ; Glioblastoma/pathology ; Glutathione/metabolism ; Humans ; Isothiocyanates/administration & dosage ; Isothiocyanates/pharmacology ; MAP Kinase Signaling System/drug effects ; Mitochondria/drug effects ; Mitochondria/metabolism ; Phosphorylation/drug effects ; Sulfoxides/administration & dosage ; Sulfoxides/pharmacology ; Tumor Hypoxia/drug effects
Chemical Substances	Antineoplastic Agents, Phytogenic ; Isothiocyanates ; Sulfoxides ; sulforaphane (GA49J4310U) ; Glutathione (GAN16C9B8O)
Language	English
Publishing date	2021-10-18
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms222011201
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Article: Back to The Fusion: Mitofusin-2 in Alzheimer's Disease.

Sita, Giulia / Hrelia, Patrizia / Graziosi, Agnese / Morroni, Fabiana

Journal of clinical medicine

2020 Volume 9, Issue 1

Abstract: Mitochondria are dynamic organelles that undergo constant fission and fusion. Mitochondria dysfunction underlies several human disorders, including Alzheimer's disease (AD). Preservation of mitochondrial dynamics is fundamental for regulating the ... ...

Abstract	Mitochondria are dynamic organelles that undergo constant fission and fusion. Mitochondria dysfunction underlies several human disorders, including Alzheimer's disease (AD). Preservation of mitochondrial dynamics is fundamental for regulating the organelle's functions. Several proteins participate in the regulation of mitochondrial morphology and networks, and among these, Mitofusin 2 (Mfn2) has been extensively studied. This review focuses on the role of Mfn2 in mitochondrial dynamics and in the crosstalk between mitochondria and the endoplasmic reticulum, in particular in AD. Understanding how this protein may be related to AD pathogenesis will provide essential information for the development of therapies for diseases linked to disturbed mitochondrial dynamics, as in AD.
Language	English
Publishing date	2020-01-02
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2662592-1
ISSN	2077-0383
ISSN	2077-0383
DOI	10.3390/jcm9010126
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Article ; Online: NLRP3 and Infections

Giulia Sita / Agnese Graziosi / Patrizia Hrelia / Fabiana Morroni

International Journal of Molecular Sciences, Vol 22, Iss 6984, p

β-Amyloid in Inflammasome beyond Neurodegeneration

2021 Volume 6984

Abstract: Amyloid beta (Aβ)-induced abnormal neuroinflammation is recognized as a major pathological feature of Alzheimer’s disease (AD), which results in memory impairment. Research exploring low-grade systemic inflammation and its impact on the development and ... ...

Abstract	Amyloid beta (Aβ)-induced abnormal neuroinflammation is recognized as a major pathological feature of Alzheimer’s disease (AD), which results in memory impairment. Research exploring low-grade systemic inflammation and its impact on the development and progression of neurodegenerative disease has increased. A particular research focus has been whether systemic inflammation arises only as a secondary effect of disease, or it is also a cause of pathology. The inflammasomes, and more specifically the NLRP3 inflammasome, are crucial components of the innate immune system and are usually activated in response to infection or tissue damage. Although inflammasome activation plays critical roles against various pathogens in host defense, overactivation of inflammasome contributes to the pathogenesis of inflammatory diseases, including acute central nervous system (CNS) injuries and chronic neurodegenerative diseases, such as AD. This review summarizes the current literature on the role of the NLRP3 inflammasome in the pathogenesis of AD, and its involvement in infections, particularly SARS-CoV-2. NLRP3 might represent the crossroad between the hypothesized neurodegeneration and the primary COVID-19 infection.
Keywords	NLRP3 ; neuroinflammation ; infections ; neurodegeneration ; Alzheimer’s disease ; COVID-19 ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	610
Language	English
Publishing date	2021-06-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Sulforaphane Causes Cell Cycle Arrest and Apoptosis in Human Glioblastoma U87MG and U373MG Cell Lines under Hypoxic Conditions

Giulia Sita / Agnese Graziosi / Patrizia Hrelia / Fabiana Morroni

International Journal of Molecular Sciences, Vol 22, Iss 11201, p

2021 Volume 11201

Abstract	Glioblastoma multiforme (GBM) is the most prevalent and aggressive primary brain tumor. The median survival rate from diagnosis ranges from 15 to 17 months because the tumor is resistant to most therapeutic strategies. GBM exhibits microvascular hyperplasia and pronounced necrosis triggered by hypoxia. Sulforaphane (SFN), an isothiocyanate derived from cruciferous vegetables, has already demonstrated the ability to inhibit cell proliferation, by provoking cell cycle arrest, and leading to apoptosis in many cell lines. In this study, we investigated the antineoplastic effects of SFN [20–80 <math xmlns="http://www.w3.org/1998/Math/MathML" display="inline"><semantics><mi mathvariant="sans-serif">μ</mi></semantics></math> M for 48 h] in GBM cells under normoxic and hypoxic conditions. Cell viability assays, flow cytometry, and Western blot results revealed that SFN could induce apoptosis of GBM cells in a dose-dependent manner, under both conditions. In particular, SFN significantly induced caspase 3/7 activation and DNA fragmentation. Moreover, our results demonstrated that SFN suppressed GBM cells proliferation by arresting the cell cycle at the S-phase, also under hypoxic condition, and that these effects may be due in part to its ability to induce oxidative stress by reducing glutathione levels and to increase the phosphorylation of extracellular signal-regulated kinases (ERKs). Overall, we hypothesized that SFN treatment might serve as a potential therapeutic strategy, alone or in combination, against GBM.
Keywords	sulforaphane ; hypoxia ; glioblastoma ; apoptosis ; U87MG ; U373MG ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	610
Language	English
Publishing date	2021-10-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: The Unfolded Protein Response in a Murine Model of Alzheimer's Disease: Looking for Predictors.

Sita, Giulia / Graziosi, Agnese / Corrieri, Camilla / Ghelli, Luca / Angelini, Sabrina / Cortelli, Pietro / Hrelia, Patrizia / Morroni, Fabiana

International journal of molecular sciences

2023 Volume 24, Issue 22

Abstract: Alzheimer's disease (AD) represents the most frequent type of dementia worldwide, and aging is the most important risk factor for the sporadic form of the pathology. The endoplasmic reticulum (ER), the main cellular actor involved in proteostasis, ... ...

Abstract	Alzheimer's disease (AD) represents the most frequent type of dementia worldwide, and aging is the most important risk factor for the sporadic form of the pathology. The endoplasmic reticulum (ER), the main cellular actor involved in proteostasis, appears significantly compromised in AD due to the accumulation of the β-amyloid (Aβ) protein and the phosphorylated Tau protein. Increasing protein misfolding activates a specific cellular response known as Unfolded Protein Response (UPR), which orchestrates the recovery of ER function. The aim of the present study was to investigate the role of UPR in a murine model of AD induced by intracerebroventricular (i.c.v.) injection of Aβ
MeSH term(s)	Mice ; Animals ; Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Protein Serine-Threonine Kinases/metabolism ; Endoribonucleases/metabolism ; Disease Models, Animal ; Phosphatidylinositol 3-Kinases/metabolism ; Unfolded Protein Response ; Endoplasmic Reticulum Stress/genetics
Chemical Substances	Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Endoribonucleases (EC 3.1.-) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-)
Language	English
Publishing date	2023-11-11
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms242216200
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Article ; Online: Back to The Fusion

Giulia Sita / Patrizia Hrelia / Agnese Graziosi / Fabiana Morroni

Journal of Clinical Medicine, Vol 9, Iss 1, p

Mitofusin-2 in Alzheimer’s Disease

2020 Volume 126

Abstract: Mitochondria are dynamic organelles that undergo constant fission and fusion. Mitochondria dysfunction underlies several human disorders, including Alzheimer’s disease (AD). Preservation of mitochondrial dynamics is fundamental for regulating the ... ...

Abstract	Mitochondria are dynamic organelles that undergo constant fission and fusion. Mitochondria dysfunction underlies several human disorders, including Alzheimer’s disease (AD). Preservation of mitochondrial dynamics is fundamental for regulating the organelle’s functions. Several proteins participate in the regulation of mitochondrial morphology and networks, and among these, Mitofusin 2 (Mfn2) has been extensively studied. This review focuses on the role of Mfn2 in mitochondrial dynamics and in the crosstalk between mitochondria and the endoplasmic reticulum, in particular in AD. Understanding how this protein may be related to AD pathogenesis will provide essential information for the development of therapies for diseases linked to disturbed mitochondrial dynamics, as in AD.
Keywords	mitofusin 2 ; alzheimer’s disease ; endoplasmic reticulum ; neuroprotection ; Medicine ; R
Language	English
Publishing date	2020-01-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Esculetin as a Bifunctional Antioxidant Prevents and Counteracts the Oxidative Stress and Neuronal Death Induced by Amyloid Protein in SH-SY5Y Cells.

Pruccoli, Letizia / Morroni, Fabiana / Sita, Giulia / Hrelia, Patrizia / Tarozzi, Andrea

Antioxidants (Basel, Switzerland)

2020 Volume 9, Issue 6

Abstract: Oxidative stress (OS) appears to be an important determinant during the different stages of progression of Alzheimer's Disease (AD). In particular, impaired antioxidant defense mechanisms, such as the decrease of glutathione (GSH) and nuclear factor ... ...

Abstract	Oxidative stress (OS) appears to be an important determinant during the different stages of progression of Alzheimer's Disease (AD). In particular, impaired antioxidant defense mechanisms, such as the decrease of glutathione (GSH) and nuclear factor erythroid 2 (NF-E2)-related factor 2 (Nrf2), a master regulator of antioxidant genes, including those for GSH, are associated with OS in the human AD brain. Among the neuropathological hallmarks of AD, the soluble oligomers of amyloid beta (A) peptides seem to promote neuronal death through mitochondrial dysfunction and OS. In this regard, bifunctional antioxidants can exert a dual neuroprotective role by scavenging reactive oxygen species (ROS) directly and concomitant induction of antioxidant genes. In this study, among natural coumarins (esculetin, scopoletin, fraxetin and daphnetin), we demonstrated the ability of esculetin (ESC) to prevent and counteract ROS formation in neuronal SH-SY5Y cells, suggesting its profile as a bifunctional antioxidant. In particular, ESC increased the resistance of the SH-SY5Y cells against OS through the activation of Nrf2 and increase of GSH. In similar experimental conditions, ESC could also protect the SH-SY5Y cells from the OS and neuronal death evoked by oligomers of A
Language	English
Publishing date	2020-06-25
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox9060551
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Article ; Online: Sulforaphane from Cruciferous Vegetables: Recent Advances to Improve Glioblastoma Treatment.

Sita, Giulia / Hrelia, Patrizia / Graziosi, Agnese / Morroni, Fabiana

Nutrients

2018 Volume 10, Issue 11

Abstract: Sulforaphane (SFN), an isothiocyanate (ITC) derived from cruciferous vegetables, particularly broccoli and broccoli sprouts, has been widely investigated due to its promising health-promoting properties in disease, and low toxicity in normal tissue. ... ...

Abstract	Sulforaphane (SFN), an isothiocyanate (ITC) derived from cruciferous vegetables, particularly broccoli and broccoli sprouts, has been widely investigated due to its promising health-promoting properties in disease, and low toxicity in normal tissue. Although not yet fully understood, many mechanisms of anticancer activity at each step of cancer development have been attributed to this ITC. Given the promising data available regarding SFN, this review aimed to provide an overview on the potential activities of SFN related to the cellular mechanisms involved in glioblastoma (GBM) progression. GBM is the most frequent malignant brain tumor among adults and is currently an incurable disease due mostly to its highly invasive phenotype, and the poor efficacy of the available therapies. Despite all efforts, the median overall survival of GBM patients remains approximately 1.5 years under therapy. Therefore, there is an urgent need to provide support for translating the progress in understanding the molecular background of GBM into more complex, but promising therapeutic strategies, in which SFN may find a leading role.
MeSH term(s)	Antineoplastic Agents, Phytogenic/chemistry ; Antineoplastic Agents, Phytogenic/pharmacology ; Brassica/chemistry ; Glioblastoma/drug therapy ; Humans ; Isothiocyanates/chemistry ; Isothiocyanates/pharmacology ; Vegetables/chemistry
Chemical Substances	Antineoplastic Agents, Phytogenic ; Isothiocyanates ; sulforaphane (GA49J4310U)
Language	English
Publishing date	2018-11-14
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2518386-2
ISSN	2072-6643 ; 2072-6643
ISSN (online)	2072-6643
ISSN	2072-6643
DOI	10.3390/nu10111755
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Sulforaphane from Cruciferous Vegetables: Recent Advances to Improve Glioblastoma Treatment

Sita, Giulia / Hrelia, Patrizia / Graziosi, Agnese / Morroni, Fabiana

Nutrients. 2018 Nov. 14, v. 10, no. 11

2018

Abstract	Sulforaphane (SFN), an isothiocyanate (ITC) derived from cruciferous vegetables, particularly broccoli and broccoli sprouts, has been widely investigated due to its promising health-promoting properties in disease, and low toxicity in normal tissue. Although not yet fully understood, many mechanisms of anticancer activity at each step of cancer development have been attributed to this ITC. Given the promising data available regarding SFN, this review aimed to provide an overview on the potential activities of SFN related to the cellular mechanisms involved in glioblastoma (GBM) progression. GBM is the most frequent malignant brain tumor among adults and is currently an incurable disease due mostly to its highly invasive phenotype, and the poor efficacy of the available therapies. Despite all efforts, the median overall survival of GBM patients remains approximately 1.5 years under therapy. Therefore, there is an urgent need to provide support for translating the progress in understanding the molecular background of GBM into more complex, but promising therapeutic strategies, in which SFN may find a leading role.
Keywords	Brassicaceae ; adults ; antineoplastic activity ; brain neoplasms ; broccoli ; carcinogenesis ; glioblastoma ; health promotion ; patients ; phenotype ; sulforaphane ; therapeutics ; toxicity
Language	English
Dates of publication	2018-1114
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2518386-2
ISSN	2072-6643
ISSN	2072-6643
DOI	10.3390/nu10111755
Database	NAL-Catalogue (AGRICOLA)

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