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Article ; Online: Microdose lithium improves behavioral deficits and modulates molecular mechanisms of memory formation in female SAMP-8, a mouse model of accelerated aging.

Pereira, Arthur Antonio Ruiz / Pinto, Alessandra Macedo / Malerba, Helena Nascimento / Toricelli, Mariana / Buck, Hudson Sousa / Viel, Tania Araujo

PloS one

2024 Volume 19, Issue 4, Page(s) e0299534

Abstract: Alzheimer's disease (AD) is the most common neuronal disorder that leads to the development of dementia. Until nowadays, some therapies may alleviate the symptoms, but there is no pharmacological treatment. Microdosing lithium has been used to modify the ...

Abstract	Alzheimer's disease (AD) is the most common neuronal disorder that leads to the development of dementia. Until nowadays, some therapies may alleviate the symptoms, but there is no pharmacological treatment. Microdosing lithium has been used to modify the pathological characteristics of the disease, with effects in both experimental and clinical conditions. The present work aimed to analyze the effects of this treatment on spatial memory, anxiety, and molecular mechanisms related to long-term memory formation during the aging process of a mouse model of accelerated aging (SAMP-8). Female SAMP-8 showed learning and memory impairments together with disruption of memory mechanisms, neuronal loss, and increased density of senile plaques compared to their natural control strain, the senescence-accelerated mouse resistant (SAMR-1). Chronic treatment with lithium promoted memory maintenance, reduction in anxiety, and maintenance of proteins related to memory formation and neuronal density. The density of senile plaques was also reduced. An increase in the density of gamma-aminobutyric acid A (GABAA) and α7 nicotinic cholinergic receptors was also observed and related to neuroprotection and anxiety reduction. In addition, this microdose of lithium inhibited the activation of glycogen synthase kinase-3beta (GSK-3β), the classical mechanism of lithium cell effects, which could contribute to the preservation of the memory mechanism and reduction in senile plaque formation. This work shows that lithium effects in neuroprotection along the aging process are not related to a unique cellular mechanism but produce multiple effects that slowly protect the brain along the aging process.
MeSH term(s)	Mice ; Female ; Animals ; Lithium/pharmacology ; Lithium/therapeutic use ; Plaque, Amyloid/pathology ; Glycogen Synthase Kinase 3 beta ; Alzheimer Disease/pathology ; Aging/metabolism ; Disease Models, Animal ; Phenylmercury Compounds
Chemical Substances	Lithium (9FN79X2M3F) ; 4-(4-sulfophenylazo)-2-mercuriphenol (69630-03-1) ; Glycogen Synthase Kinase 3 beta (EC 2.7.11.1) ; Phenylmercury Compounds
Language	English
Publishing date	2024-04-04
Publishing country	United States
Document type	Journal Article
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0299534
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Article ; Online: Microdose Lithium Treatment Reduced Inflammatory Factors and Neurodegeneration in Organotypic Hippocampal Culture of Old SAMP-8 Mice.

Toricelli, Mariana / Evangelista, Sebastiana Ribeiro / Buck, Hudson Sousa / Viel, Tania Araujo

Cellular and molecular neurobiology

2020 Volume 41, Issue 7, Page(s) 1509–1520

Abstract: It was already shown that microdoses of lithium carbonate ( ... ...

Abstract	It was already shown that microdoses of lithium carbonate (Li
MeSH term(s)	Alzheimer Disease/drug therapy ; Alzheimer Disease/metabolism ; Animals ; Cell Death/drug effects ; Disease Models, Animal ; Hippocampus/drug effects ; Hippocampus/metabolism ; Lithium/pharmacology ; Mice, Transgenic ; Neurons/drug effects ; Neurons/metabolism ; Neuroprotective Agents/pharmacology ; Phenylmercury Compounds/pharmacology
Chemical Substances	Neuroprotective Agents ; Phenylmercury Compounds ; 4-(4-sulfophenylazo)-2-mercuriphenol (69630-03-1) ; Lithium (9FN79X2M3F)
Language	English
Publishing date	2020-07-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	283404-2
ISSN	1573-6830 ; 0272-4340
ISSN (online)	1573-6830
ISSN	0272-4340
DOI	10.1007/s10571-020-00916-0
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Article: Combined Neuroprotective Strategies Blocked Neurodegeneration and Improved Brain Function in Senescence-Accelerated Mice.

Malerba, Helena Nascimento / Pereira, Arthur Antonio Ruiz / Pierrobon, Marcela Favoretto / Abrao, Guilherme Souza / Toricelli, Mariana / Akamine, Eliana Hiromi / Buck, Hudson Sousa / Viel, Tania Araujo

Frontiers in aging neuroscience

2021 Volume 13, Page(s) 681498

Abstract: Increase in the quality of life, combined with drug strategies, has been studied as possibilities for improving memory and delaying the onset of neurodegenerative diseases. A previous study published by the group of the authors has shown that microdose ... ...

Abstract	Increase in the quality of life, combined with drug strategies, has been studied as possibilities for improving memory and delaying the onset of neurodegenerative diseases. A previous study published by the group of the authors has shown that microdose lithium and enriched environment can improve memory in both mice and humans. To elucidate this relationship better, this study aimed to evaluate whether the chronic combination of these two strategies could increase healthy aging in Senescence Accelerated Mouse-Prone 8 (SAMP8). Animals were submitted to either one or both of these strategies until the age of 10 months when they were anesthetized and killed and their hippocampus was extracted. The untreated SAMP-8 group exhibited worse memory and reduced neuronal density with greater neurodegeneration and increased amyloid-β plaque density compared with the control group. Moreover, significant alterations in proteins related to long-term potentiation, such as, synaptophysin and brain-derived neurotrophic factor (BDNF), were observed in this group. The strategies used in the study maintained long-term memory, reduced anxiety, and increased neuroprotection. Both strategies were efficient in reducing neurodegeneration and increasing parameters related to memory maintenance. In many experiments, the combination of the two strategies was more effective in improving healthy aging. This study sheds light on the combination of strategies that choose to improve the quality of life and drugs with low side effects. Moreover, it opens perspectives for a new field of study for healthy aging.
Language	English
Publishing date	2021-08-23
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2558898-9
ISSN	1663-4365
ISSN	1663-4365
DOI	10.3389/fnagi.2021.681498
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Article: Neuroprotective Effects of Kinin B2 Receptor in Organotypic Hippocampal Cultures of Middle-Aged Mice.

Toricelli, Mariana / Evangelista, Sebastiana Ribeiro / Oliveira, Larissa Rolim / Viel, Tania Araujo / Buck, Hudson Sousa

Frontiers in aging neuroscience

2019 Volume 11, Page(s) 168

Abstract: Aging is a multifactorial phenomenon that results in several changes at cellular and molecular levels and is considered the main risk factor for some neurodegenerative diseases. Several evidence show the participation of the kallikrein-kinin system (KKS) ...

Abstract	Aging is a multifactorial phenomenon that results in several changes at cellular and molecular levels and is considered the main risk factor for some neurodegenerative diseases. Several evidence show the participation of the kallikrein-kinin system (KKS) in neurodegeneration and this system has been associated with inflammation and immunogenic responses in the central and peripheral systems by the activation of the B1 and B2 receptors. Previous work by our group showed that bradykinin (BK) and the B2 receptor played a possible role in neuroprotection. Therefore, the objective of this study was to evaluate the participation of B2 receptors in cell viability, neuroinflammatory response and neuroplasticity in organotypic hippocampal cultures (OHCs) of 6- and 12-month-old mice. It was observed that activation of the B2 receptor by bradykinin decreased the inflammatory response and increased plasticity in 12-month-old slices. Conversely, there was an increase in the inflammatory response and a decrease in neural plasticity in the 6-month-old slices. In both ages, an increase in cell viability was observed. This data suggests that the function of the kinin B2 receptor in the hippocampus is modulated by age, providing neuroprotective action in old age.
Language	English
Publishing date	2019-07-12
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2558898-9
ISSN	1663-4365
ISSN	1663-4365
DOI	10.3389/fnagi.2019.00168
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Article: Mechanisms of neuroplasticity and brain degeneration: strategies for protection during the aging process.

Toricelli, Mariana / Pereira, Arthur Antonio Ruiz / Souza Abrao, Guilherme / Malerba, Helena Nascimento / Maia, Julia / Buck, Hudson Sousa / Viel, Tania Araujo

Neural regeneration research

2020 Volume 16, Issue 1, Page(s) 58–67

Abstract: Aging is a dynamic and progressive process that begins at conception and continues until death. This process leads to a decrease in homeostasis and morphological, biochemical and psychological changes, increasing the individual's vulnerability to various ...

Abstract	Aging is a dynamic and progressive process that begins at conception and continues until death. This process leads to a decrease in homeostasis and morphological, biochemical and psychological changes, increasing the individual's vulnerability to various diseases. The growth in the number of aging populations has increased the prevalence of chronic degenerative diseases, impairment of the central nervous system and dementias, such as Alzheimer's disease, whose main risk factor is age, leading to an increase of the number of individuals who need daily support for life activities. Some theories about aging suggest it is caused by an increase of cellular senescence and reactive oxygen species, which leads to inflammation, oxidation, cell membrane damage and consequently neuronal death. Also, mitochondrial mutations, which are generated throughout the aging process, can lead to changes in energy production, deficiencies in electron transport and apoptosis induction that can result in decreased function. Additionally, increasing cellular senescence and the release of proinflammatory cytokines can cause irreversible damage to neuronal cells. Recent reports point to the importance of changing lifestyle by increasing physical exercise, improving nutrition and environmental enrichment to activate neuroprotective defense mechanisms. Therefore, this review aims to address the latest information about the different mechanisms related to neuroplasticity and neuronal death and to provide strategies that can improve neuroprotection and decrease the neurodegeneration caused by aging and environmental stressors.
Language	English
Publishing date	2020-08-11
Publishing country	India
Document type	Journal Article
ZDB-ID	2388460-5
ISSN	1876-7958 ; 1673-5374
ISSN (online)	1876-7958
ISSN	1673-5374
DOI	10.4103/1673-5374.286952
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Article: Timp1 Promotes Cell Survival by Activating the PDK1 Signaling Pathway in Melanoma.

Toricelli, Mariana / Melo, Fabiana H M / Hunger, Aline / Zanatta, Daniela / Strauss, Bryan E / Jasiulionis, Miriam G

Cancers

2017 Volume 9, Issue 4

Abstract: High TIMP1 expression is associated with poor prognosis in melanoma, where it can bind to CD63 and β1 integrin, inducing PI3-kinase pathway and cell survival. Phosphatidylinositol (3,4,5)-trisphosphate (PIP3), generated under phosphatidylinositol-3- ... ...

Abstract	High TIMP1 expression is associated with poor prognosis in melanoma, where it can bind to CD63 and β1 integrin, inducing PI3-kinase pathway and cell survival. Phosphatidylinositol (3,4,5)-trisphosphate (PIP3), generated under phosphatidylinositol-3-kinase (PI3K) activation, enables the recruitment and activation of protein kinase B (PKB/AKT) and phosphoinositide-dependent kinase 1 (PDK1) at the membrane, resulting in the phosphorylation of a host of other proteins. Using a melanoma progression model, we evaluated the impact of Timp1 and AKT silencing, as well as PI3K, PDK1, and protein kinase C (PKC) inhibitors on aggressiveness characteristics. Timp1 downregulation resulted in decreased
Language	English
Publishing date	2017-04-21
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers9040037
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Article: Kinin B2 Receptor Activation Prevents the Evolution of Alzheimer's Disease Pathological Characteristics in a Transgenic Mouse Model.

Nunes, Marielza Andrade / Toricelli, Mariana / Schöwe, Natalia Mendes / Malerba, Helena Nascimento / Dong-Creste, Karis Ester / Farah, Daniela Moura Azevedo Tuma / De Angelis, Katia / Irigoyen, Maria Claudia / Gobeil, Fernand / Araujo Viel, Tânia / Buck, Hudson Sousa

Pharmaceuticals (Basel, Switzerland)

2020 Volume 13, Issue 10

Abstract: Background: Alzheimer's disease is mainly characterized by remarkable neurodegeneration in brain areas related to memory formation. This progressive neurodegeneration causes cognitive impairment, changes in behavior, functional disability, and even ... ...

Abstract	Background: Alzheimer's disease is mainly characterized by remarkable neurodegeneration in brain areas related to memory formation. This progressive neurodegeneration causes cognitive impairment, changes in behavior, functional disability, and even death. Our group has demonstrated changes in the kallikrein-kinin system (KKS) in Alzheimer's disease (AD) experimental models, but there is a lack of evidence about the role of the KKS in Alzheimer's disease. Aim: In order to answer this question, we evaluated the potential of the kinin B2 receptors (BKB2R) to modify AD characteristics, particularly memory impairment, neurodegeneration, and Aβ peptide deposition. Methods: To assess the effects of B2, we used transgenic Alzheimer's disease mice treated with B2 receptor (B2R) agonists and antagonists, and performed behavioral and biochemical tests. In addition, we performed organotypic hippocampal culture of wild-type (WT) and transgenic (TG) animals, where the density of cytokines, neurotrophin BDNF, activated astrocyte marker S100B, and cell death were analyzed after treatments. Results: Treatment with the B2R agonist preserved the spatial memory of transgenic mice and decreased amyloid plaque deposition. In organotypic hippocampal culture, treatment with B2R agonist decreased cell death, neuroinflammation, and S100B levels, and increased BDNF release. Conclusions: Our results indicate that the kallikrein-kinin system plays a beneficial role in Alzheimer's disease through B2R activation. The use of B2R agonists could, therefore, be a possible therapeutic option for patients diagnosed with Alzheimer's disease.
Language	English
Publishing date	2020-10-01
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2193542-7
ISSN	1424-8247
ISSN	1424-8247
DOI	10.3390/ph13100288
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Article ; Online: Erratum: Timp1 interacts with beta-1 integrin and CD63 along melanoma genesis and confers anoikis resistance by activating PI3-K signaling pathway independently of Akt phosphorylation.

Toricelli, Mariana / Melo, Fabiana H M / Peres, Giovani B / Silva, Débora C P / Jasiulionis, Miriam G

Molecular cancer

2015 Volume 14, Page(s) 161

Language	English
Publishing date	2015-08-22
Publishing country	England
Document type	Published Erratum
ISSN	1476-4598
ISSN (online)	1476-4598
DOI	10.1186/s12943-015-0405-2
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Article ; Online: Timp1 interacts with beta-1 integrin and CD63 along melanoma genesis and confers anoikis resistance by activating PI3-K signaling pathway independently of Akt phosphorylation.

Toricelli, Mariana / Melo, Fabiana H M / Peres, Giovani B / Silva, Débora C P / Jasiulionis, Miriam G

Molecular cancer

2013 Volume 12, Page(s) 22

Abstract: Background: Anoikis resistance is one of the abilities acquired along tumor progression. This characteristic is associated with metastasis development, since tumorigenic cells must survive independently of cell-matrix interactions in this process. In ... ...

Abstract	Background: Anoikis resistance is one of the abilities acquired along tumor progression. This characteristic is associated with metastasis development, since tumorigenic cells must survive independently of cell-matrix interactions in this process. In our laboratory, it was developed a murine melanocyte malignant transformation model associated with a sustained stressful condition. After subjecting melan-a melanocytes to 1, 2, 3 and 4 cycles of anchorage impediment, anoikis resistant cells were established and named 1C, 2C, 3C and 4C, respectively. These cells showed altered morphology and PMA independent cell growth, but were not tumorigenic, corresponding to pre-malignant cells. After limiting dilution of 4C pre-malignant cells, melanoma cell lines with different characteristics were obtained. Previous data from our group showed that increased Timp1 expression correlated with anoikis-resistant phenotype. Timp1 was shown to confer anchorage-independent growth capability to melan-a melanocytes and render melanoma cells more aggressive when injected into mice. However, the mechanisms involved in anoikis regulation by Timp1 in tumorigenic cells are not clear yet. Methods: The β1-integrin and Timp1 expression were evaluated by Western blotting and CD63 protein expression by flow cytometry using specific antibodies. To analyze the interaction among Timp1, CD63 and β1-integrin, immunoprecipitation assays were performed, anoikis resistance capability was evaluated in the presence or not of the PI3-K inhibitors, Wortmannin and LY294002. Relative expression of TIMP1 and CD63 in human metastatic melanoma cells was analyzed by real time PCR. Results: Differential association among Timp1, CD63 and β1-integrins was observed in melan-a melanocytes, 4C pre-malignant melanocytes and 4C11- and 4C11+ melanoma cells. Timp1 present in conditioned medium of melanoma cells rendered melan-a melanocytes anoikis-resistant through PI3-K signaling pathway independently of Akt activation. In human melanoma cell lines, in which TIMP1 and beta-1 integrin were also found to be interacting, TIMP1 and CD63 levels together was shown to correlate significantly with colony formation capacity. Conclusions: Our results show that Timp1 is assembled in a supramolecular complex containing CD63 and β1-integrins along melanoma genesis and confers anoikis resistance by activating PI3-K signaling pathway, independently of Akt phosphorylation. In addition, our data point TIMP1, mainly together with CD63, as a potential biomarker of melanoma.
MeSH term(s)	Anoikis/drug effects ; Anoikis/genetics ; Cell Line ; Cell Survival/drug effects ; Cell Survival/genetics ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/metabolism ; Culture Media, Conditioned/chemistry ; Culture Media, Conditioned/pharmacology ; Disease Progression ; Gene Expression ; Humans ; Integrin beta1/metabolism ; MART-1 Antigen/metabolism ; Melanocytes/drug effects ; Melanocytes/metabolism ; Melanocytes/pathology ; Melanoma/genetics ; Melanoma/metabolism ; Melanoma/pathology ; Models, Biological ; Multiprotein Complexes/metabolism ; Neoplasm Metastasis ; Phenotype ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphoinositide-3 Kinase Inhibitors ; Phosphorylation ; Protein Binding ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction ; Tetraspanin 30/metabolism ; Tissue Inhibitor of Metalloproteinase-1/genetics ; Tissue Inhibitor of Metalloproteinase-1/metabolism ; Tissue Inhibitor of Metalloproteinase-1/pharmacology
Chemical Substances	Culture Media, Conditioned ; Integrin beta1 ; MART-1 Antigen ; Multiprotein Complexes ; Phosphoinositide-3 Kinase Inhibitors ; Tetraspanin 30 ; Tissue Inhibitor of Metalloproteinase-1 ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2013-03-25
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1476-4598
ISSN (online)	1476-4598
DOI	10.1186/1476-4598-12-22
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Article ; Online: Endothelial nitric oxide synthase uncoupling as a key mediator of melanocyte malignant transformation associated with sustained stress conditions.

Melo, Fabiana H M / Molognoni, Fernanda / Morais, Alice S / Toricelli, Mariana / Mouro, Margareth G / Higa, Elisa M S / Lopes, José D / Jasiulionis, Miriam G

Free radical biology & medicine

2011 Volume 50, Issue 10, Page(s) 1263–1273

Abstract: Melanoma cell lines and cells corresponding to premalignant melanocytes were established by our group after subjecting a nontumorigenic murine melanocyte lineage, melan-a, to sequential cycles of anchorage blockade. Previous results showed that in melan- ... ...

Abstract	Melanoma cell lines and cells corresponding to premalignant melanocytes were established by our group after subjecting a nontumorigenic murine melanocyte lineage, melan-a, to sequential cycles of anchorage blockade. Previous results showed that in melan-a cells the superoxide level increases after such procedure. Superoxide production during melanocyte de-adhesion was inhibited by L-sepiapterin, the precursor of eNOS cofactor BH4, and increased by the inhibitor of BH4 synthesis, DAHP, hence indicating a partial uncoupling state of eNOS. The eNOS uncoupling seems to be maintained in cells derived from melan-a, because they present decreased nitric oxide and increased superoxide levels. The inhibition of superoxide production in Tm5 melanoma cells with L-sepiapterin reinforces their eNOS-uncoupled state. The maintenance of oxidative stress seems to be important in melanoma apoptosis resistance because Mn(III)TBAP, a superoxide scavenger, or L-sepiapterin renders Tm5 cells more sensitive to anoikis and chemotherapy. More importantly, eNOS uncoupling seems to play a pivotal role in melanocyte malignant transformation induced by sustained anchorage impediment, because no malignant transformation was observed when L-NAME-treated melanocytes were subjected to sequential cycles of de-adhesion. Our results show that uncoupled eNOS contributes to superoxide production during melanocyte anchorage impediment, contributing to anoikis resistance and malignant transformation.
MeSH term(s)	Animals ; Melanocytes/drug effects ; Melanocytes/metabolism ; Melanocytes/pathology ; Mice ; NG-Nitroarginine Methyl Ester/pharmacology ; Nitric Oxide Synthase Type III/metabolism ; Oxidative Stress/drug effects ; Superoxides/metabolism ; Tumor Cells, Cultured
Chemical Substances	Superoxides (11062-77-4) ; Nitric Oxide Synthase Type III (EC 1.14.13.39) ; NG-Nitroarginine Methyl Ester (V55S2QJN2X)
Language	English
Publishing date	2011-05-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	807032-5
ISSN	1873-4596 ; 0891-5849
ISSN (online)	1873-4596
ISSN	0891-5849
DOI	10.1016/j.freeradbiomed.2011.02.022
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