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Article ; Online: Aging changes the expression of adenosine receptors, insulin-like growth factor 1 (IGF1), and hypoxia-inducible factor 1α (HIF1α) in hypothalamic astrocyte cultures.

Santos, Camila Leite / Bobermin, Larissa Daniele / Quincozes-Santos, André

Aging brain

2023 Volume 5, Page(s) 100104

Abstract: The aging process induces neurochemical alterations in different brain regions, including hypothalamus. This pivotal area of the central nervous system (CNS) is crucial for detection and integration of nutritional and hormonal signals from the periphery ... ...

Abstract	The aging process induces neurochemical alterations in different brain regions, including hypothalamus. This pivotal area of the central nervous system (CNS) is crucial for detection and integration of nutritional and hormonal signals from the periphery of the body to maintain metabolic homeostasis. Astrocytes support the CNS homeostasis, energy metabolism, and inflammatory response, as well as increasing evidence has highlighted a critical role of astrocytes in orchestrating hypothalamic functions and in gliocrine system. In this study, we aimed to investigate the age-dependent mRNA expression of adenosine receptors, the insulin-like growth factor 1 receptor (IGF1R), and the hypoxia-inducible factor 1α (HIF1α), in addition to the levels of IGF1 and HIF1α in hypothalamic astrocyte cultures derived from newborn, adult, and aged rats. Our results revealed age-dependent changes in adenosine receptors, as well as a decrease in IGF1R/IGF1 and HIF1α. Of note, adenosine receptors, IGF1, and HIF1α are affected by inflammatory, redox, and metabolic processes, which can remodel hypothalamic properties, as observed in aging brain, reinforcing the role of hypothalamic astrocytes as targets for understanding the onset and/or progression of age-related diseases.
Language	English
Publishing date	2023-12-23
Publishing country	Netherlands
Document type	Journal Article
ISSN	2589-9589
ISSN (online)	2589-9589
DOI	10.1016/j.nbas.2023.100104
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Article ; Online: Differences between cultured astrocytes from neonatal and adult Wistar rats: focus on in vitro aging experimental models.

Weber, Fernanda Becker / Santos, Camila Leite / da Silva, Amanda / Schmitz, Izaviany / Rezena, Ester / Gonçalves, Carlos-Alberto / Quincozes-Santos, André / Bobermin, Larissa Daniele

In vitro cellular & developmental biology. Animal

2024

Abstract: Astrocytes play key roles regulating brain homeostasis and accumulating evidence has suggested that glia are the first cells that undergo functional changes with aging, which can lead to a decline in brain function. In this context, in vitro models are ... ...

Abstract	Astrocytes play key roles regulating brain homeostasis and accumulating evidence has suggested that glia are the first cells that undergo functional changes with aging, which can lead to a decline in brain function. In this context, in vitro models are relevant tools for studying aged astrocytes and, here, we investigated functional and molecular changes in cultured astrocytes obtained from neonatal or adult animals submitted to an in vitro model of aging by an additional period of cultivation of cells after confluence. In vitro aging induced different metabolic effects regarding glucose and glutamate uptake, as well as glutamine synthetase activity, in astrocytes obtained from adult animals compared to those obtained from neonatal animals. In vitro aging also modulated glutathione-related antioxidant defenses and increased reactive oxygen species and cytokine release especially in astrocytes from adult animals. Interestingly, in vitro aged astrocytes from adult animals exposed to pro-oxidant, inflammatory, and antioxidant stimuli showed enhanced oxidative and inflammatory responses. Moreover, these functional changes were correlated with the expression of the senescence marker p21, cytoskeleton markers, glutamate transporters, inflammatory mediators, and signaling pathways such as nuclear factor κB (NFκB)/nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1). Alterations in these genes are remarkably associated with a potential neurotoxic astrocyte phenotype. Therefore, considering the experimental limitations due to the need for long-term maintenance of the animals for studying aging, astrocyte cultures obtained from adult animals further aged in vitro can provide an improved experimental model for understanding the mechanisms associated with aging-related astrocyte dysfunction.
Language	English
Publishing date	2024-03-28
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1077810-x
ISSN	1543-706X ; 0883-8364 ; 1071-2690
ISSN (online)	1543-706X
ISSN	0883-8364 ; 1071-2690
DOI	10.1007/s11626-024-00896-1
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Zs.A 851: Show issues

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Article ; Online: COVID-19 and hyperammonemia: Potential interplay between liver and brain dysfunctions.

Bobermin, Larissa Daniele / Quincozes-Santos, André

Brain, behavior, & immunity - health

2021 Volume 14, Page(s) 100257

Abstract: Although COVID-19 affects the respiratory system, extrapulmonary manifestations frequently occur, including encephalopathy and liver damage. Here, we want to call attention to a possible connection between liver and brain dysfunctions, in which ammonia ... ...

Abstract	Although COVID-19 affects the respiratory system, extrapulmonary manifestations frequently occur, including encephalopathy and liver damage. Here, we want to call attention to a possible connection between liver and brain dysfunctions, in which ammonia can play a role targeting astrocytes. Importantly, astrocyte dysfunction can produce future and/or long-term neurological consequences.
Language	English
Publishing date	2021-04-13
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2666-3546
ISSN (online)	2666-3546
DOI	10.1016/j.bbih.2021.100257
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Article ; Online: The Janus face of antipsychotics in glial cells: Focus on glioprotection.

Schmitz, Izaviany / da Silva, Amanda / Bobermin, Larissa Daniele / Gonçalves, Carlos-Alberto / Steiner, Johann / Quincozes-Santos, André

Experimental biology and medicine (Maywood, N.J.)

2024 Volume 248, Issue 22, Page(s) 2120–2130

Abstract: Antipsychotics are commonly prescribed to treat several neuropsychiatric disorders, including schizophrenia, mania in bipolar disorder, autism spectrum disorder, delirium, and organic or secondary psychosis, for example, in dementias such as Alzheimer's ... ...

Abstract	Antipsychotics are commonly prescribed to treat several neuropsychiatric disorders, including schizophrenia, mania in bipolar disorder, autism spectrum disorder, delirium, and organic or secondary psychosis, for example, in dementias such as Alzheimer's disease. There is evidence that typical antipsychotics such as haloperidol are more effective in reducing positive symptoms than negative symptoms and/or cognitive deficits. In contrast, atypical antipsychotic agents have gained popularity over typical antipsychotics, due to fewer extrapyramidal side effects and their theoretical efficacy in controlling both positive and negative symptoms. Although these therapies focus on neuron-based therapeutic schemes, glial cells have been recognized as important regulators of the pathophysiology of neuropsychiatric disorders, as well as targets to improve the efficacy of these drugs. Glial cells (astrocytes, oligodendrocytes, and microglia) are critical for the central nervous system in both physiological and pathological conditions. Astrocytes are the most abundant glial cells and play important roles in brain homeostasis, regulating neurotransmitter systems and gliotransmission, since they express a wide variety of functional receptors for different neurotransmitters. In addition, converging lines of evidence indicate that psychiatric disorders are commonly associated with the triad neuroinflammation, oxidative stress, and excitotoxicity, and that glial cells may contribute to the gliotoxicity process. Conversely, glioprotective molecules attenuate glial damage by generating specific responses that can protect glial cells themselves and/or neurons, resulting in improved central nervous system (CNS) functioning. In this regard, resveratrol is well-recognized as a glioprotective molecule, including in clinical studies of schizophrenia and autism. This review will provide a summary of the dual role of antipsychotics on neurochemical parameters associated with glial functions and will highlight the potential activity of glioprotective molecules to improve the action of antipsychotics.
MeSH term(s)	Humans ; Antipsychotic Agents/adverse effects ; Autism Spectrum Disorder/chemically induced ; Autism Spectrum Disorder/drug therapy ; Haloperidol/therapeutic use ; Schizophrenia/drug therapy ; Schizophrenia/chemically induced ; Neuroglia
Chemical Substances	Antipsychotic Agents ; Haloperidol (J6292F8L3D)
Language	English
Publishing date	2024-01-17
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	4015-0
ISSN	1535-3699 ; 1525-1373 ; 0037-9727
ISSN (online)	1535-3699 ; 1525-1373
ISSN	0037-9727
DOI	10.1177/15353702231222027
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Ua VI Zs.111: Show issues

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Article: TOM70 in Glial Cells as a Potential Target for Treatment of COVID-19.

Montenegro, Yorran Hardman Araújo / Zanatta, Geancarlo / Quincozes-Santos, André / Leipnitz, Guilhian

Frontiers in cellular neuroscience

2021 Volume 15, Page(s) 811376

Language	English
Publishing date	2021-12-24
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2452963-1
ISSN	1662-5102
ISSN	1662-5102
DOI	10.3389/fncel.2021.811376
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Article ; Online: Age-dependent effects of resveratrol in hypothalamic astrocyte cultures.

Leite Santos, Camila / K Vizuete, Adriana Fernanda / Becker Weber, Fernanda / Thomaz, Natalie K / Bobermin, Larissa Daniele / Gonçalves, Carlos-Alberto / Quincozes-Santos, André

Neuroreport

2023 Volume 34, Issue 8, Page(s) 419–425

Abstract: Objectives: The hypothalamus plays critical roles in maintaining brain homeostasis and increasing evidence has highlighted astrocytes orchestrating several of hypothalamic functions. However, it remains unclear how hypothalamic astrocytes participate in ...

Abstract	Objectives: The hypothalamus plays critical roles in maintaining brain homeostasis and increasing evidence has highlighted astrocytes orchestrating several of hypothalamic functions. However, it remains unclear how hypothalamic astrocytes participate in neurochemical mechanisms associated with aging process, as well as whether these cells can be a target for antiaging strategies. In this sense, the aim of this study is to evaluate the age-dependent effects of resveratrol, a well-characterized neuroprotective compound, in primary astrocyte cultures derived from the hypothalamus of newborn, adult, and aged rats. Methods: Male Wistar rats (2, 90, 180, and 365 days old) were used in this study. Cultured astrocytes from different ages were treated with 10 and 100 μM resveratrol and cellular viability, metabolic activity, astrocyte morphology, release of glial cell line-derived neurotrophic factor (GDNF), transforming growth factor β (TGF-β), tumor necrosis factor α (TNF-α), interleukins (IL-1β, IL-6, and IL-10), as well as the protein levels of Nrf2 and HO-1 were evaluated. Results: In vitro astrocytes derived from neonatal, adults, and aged animals changed metabolic activity and the release of trophic factors (GDNF and TGF-β), as well as the inflammatory mediators (TNF-α, IL-1β, IL-6, and IL-10). Resveratrol prevented these alterations. In addition, resveratrol changed the immunocontent of Nrf2 and HO-1. The results indicated that the effects of resveratrol seem to have a dose- and age-associated glioprotective role. Conclusion: These findings demonstrate for the first time that resveratrol prevents the age-dependent underlying functional reprogramming of in vitro hypothalamic astrocytes, reinforcing its antiaging activity, and consequently, its glioprotective role.
MeSH term(s)	Rats ; Animals ; Male ; Resveratrol/pharmacology ; Astrocytes/metabolism ; Rats, Wistar ; Interleukin-10/pharmacology ; Glial Cell Line-Derived Neurotrophic Factor/metabolism ; Glial Cell Line-Derived Neurotrophic Factor/pharmacology ; Tumor Necrosis Factor-alpha/metabolism ; NF-E2-Related Factor 2/metabolism ; Interleukin-6/metabolism ; Hypothalamus/metabolism ; Transforming Growth Factor beta/metabolism ; Cells, Cultured
Chemical Substances	Resveratrol (Q369O8926L) ; Interleukin-10 (130068-27-8) ; Glial Cell Line-Derived Neurotrophic Factor ; Tumor Necrosis Factor-alpha ; NF-E2-Related Factor 2 ; Interleukin-6 ; Transforming Growth Factor beta
Language	English
Publishing date	2023-04-25
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1049746-8
ISSN	1473-558X ; 0959-4965
ISSN (online)	1473-558X
ISSN	0959-4965
DOI	10.1097/WNR.0000000000001906
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Zs.A 3118: Show issues

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Article ; Online: Effect of metformin in hypothalamic astrocytes from an immunocompromised mice model.

Bobermin, Larissa Daniele / da Costa, Daniele Schauren / de Moraes, Aline Daniel Moreira / da Silva, Vanessa Fernanda / de Oliveira, Giancarlo Tomazzoni / Sesterheim, Patrícia / Tramontina, Ana Carolina / Basso, Luiz Augusto / Leipnitz, Guilhian / Quincozes-Santos, André / Gonçalves, Carlos-Alberto

Biochimie

2024

Abstract: Astrocytes are glial cells that play key roles in neuroinflammation, which is a common feature in diabetic encephalopathy and aging process. Metformin is an antidiabetic compound that shows neuroprotective properties, including in inflammatory models, ... ...

Abstract	Astrocytes are glial cells that play key roles in neuroinflammation, which is a common feature in diabetic encephalopathy and aging process. Metformin is an antidiabetic compound that shows neuroprotective properties, including in inflammatory models, but astroglial signaling pathways involved are still poorly known. Interferons α/β are cytokines that participate in antiviral responses and the lack of their signaling increases susceptible to viral infections. Here, we investigated the effects of metformin on astrocytes from hypothalamus, a crucial brain region related to inflammatory processes. Astrocyte cultures were derived from interferon α/β receptor knockout (IFNα/βR
Language	English
Publishing date	2024-04-18
Publishing country	France
Document type	Journal Article
ZDB-ID	120345-9
ISSN	1638-6183 ; 0300-9084
ISSN (online)	1638-6183
ISSN	0300-9084
DOI	10.1016/j.biochi.2024.04.005
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Article ; Online: Homocysteine and Gliotoxicity.

Wyse, Angela T S / Bobermin, Larissa Daniele / Dos Santos, Tiago Marcon / Quincozes-Santos, André

Neurotoxicity research

2021 Volume 39, Issue 3, Page(s) 966–974

Abstract: Homocysteine is a sulfur amino acid that does not occur in the diet, but it is an essential intermediate in normal mammalian metabolism of methionine. Hyperhomocysteinemia results from dietary intakes of Met, folate, and vitamin B12 and lifestyle or from ...

Abstract	Homocysteine is a sulfur amino acid that does not occur in the diet, but it is an essential intermediate in normal mammalian metabolism of methionine. Hyperhomocysteinemia results from dietary intakes of Met, folate, and vitamin B12 and lifestyle or from the deficiency of specific enzymes, leading to tissue accumulation of this amino acid and/or its metabolites. Severe hyperhomocysteinemic patients can present neurological symptoms and structural brain abnormalities, of which the pathogenesis is poorly understood. Moreover, a possible link between homocysteine (mild hyperhomocysteinemia) and neurodegenerative/neuropsychiatric disorders has been suggested. In recent years, increasing evidence has emerged suggesting that astrocyte dysfunction is involved in the neurotoxicity of homocysteine and possibly associated with the physiopathology of hyperhomocysteinemia. This review addresses some of the findings obtained from in vivo and in vitro experimental models, indicating high homocysteine levels as an important neurotoxin determinant of the neuropathophysiology of brain damage. Recent data show that this amino acid impairs glutamate uptake, redox/mitochondrial homeostasis, inflammatory response, and cell signaling pathways. Therefore, the discussion of this review focuses on homocysteine-induced gliotoxicity, and its impacts in the brain functions. Through understanding the Hcy-induced gliotoxicity, novel preventive/therapeutic strategies might emerge for these diseases.
MeSH term(s)	Animals ; Astrocytes/drug effects ; Astrocytes/metabolism ; Astrocytes/pathology ; Gliosis/chemically induced ; Gliosis/metabolism ; Gliosis/pathology ; Homocysteine/metabolism ; Homocysteine/toxicity ; Humans ; Hyperhomocysteinemia/chemically induced ; Hyperhomocysteinemia/metabolism ; Hyperhomocysteinemia/pathology ; Neurodegenerative Diseases/chemically induced ; Neurodegenerative Diseases/metabolism ; Neurodegenerative Diseases/pathology ; Neuroglia/drug effects ; Neuroglia/metabolism ; Neuroglia/pathology
Chemical Substances	Homocysteine (0LVT1QZ0BA)
Language	English
Publishing date	2021-03-30
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2036826-4
ISSN	1476-3524 ; 1029-8428
ISSN (online)	1476-3524
ISSN	1029-8428
DOI	10.1007/s12640-021-00359-5
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Zs.A 5749: Show issues

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Article ; Online: Mild Hyperhomocysteinemia Causes Anxiety-like Behavior and Brain Hyperactivity in Rodents: Are ATPase and Excitotoxicity by NMDA Receptor Overstimulation Involved in this Effect?

Dos Santos, Tiago Marcon / Siebert, Cassiana / Bobermin, Larissa Daniele / Quincozes-Santos, André / Wyse, Angela T S

Cellular and molecular neurobiology

2021 Volume 42, Issue 8, Page(s) 2697–2714

Abstract: Mild hyperhomocysteinemia is a risk factor for psychiatric and neurodegenerative diseases, whose mechanisms between them are not well-known. In the present study, we evaluated the emotional behavior and neurochemical pathways (ATPases, glutamate ... ...

Abstract	Mild hyperhomocysteinemia is a risk factor for psychiatric and neurodegenerative diseases, whose mechanisms between them are not well-known. In the present study, we evaluated the emotional behavior and neurochemical pathways (ATPases, glutamate homeostasis, and cell viability) in amygdala and prefrontal cortex rats subjected to mild hyperhomocysteinemia (in vivo studies). The ex vivo effect of homocysteine on ATPases and redox status, as well as on NMDAR antagonism by MK-801 in same structures slices were also performed. Wistar male rats received a subcutaneous injection of 0.03 µmol Homocysteine/g of body weight or saline, twice a day from 30 to 60th-67th days of life. Hyperhomocysteinemia increased anxiety-like behavior and tended to alter locomotion/exploration of rats, whereas sucrose preference and forced swimming tests were not altered. Glutamate uptake was not changed, but the activities of glutamine synthetase and ATPases were increased. Cell viability was not altered. Ex vivo studies (slices) showed that homocysteine altered ATPases and redox status and that MK801, an NMDAR antagonist, protected amygdala (partially) and prefrontal cortex (totally) effects. Taken together, data showed that mild hyperhomocysteinemia impairs the emotional behavior, which may be associated with changes in ATPase and glutamate homeostasis, including glutamine synthetase and NMDAR overstimulation that could lead to excitotoxicity. These findings may be associated with the homocysteine risk factor on psychiatric disorders development and neurodegeneration.
MeSH term(s)	Animals ; Anxiety ; Brain/metabolism ; Dizocilpine Maleate/pharmacology ; Glutamate-Ammonia Ligase/metabolism ; Glutamic Acid/metabolism ; Homocysteine ; Hyperhomocysteinemia/complications ; Hyperhomocysteinemia/metabolism ; Male ; Rats ; Rats, Wistar ; Receptors, N-Methyl-D-Aspartate/metabolism ; Rodentia/metabolism ; Sodium-Potassium-Exchanging ATPase/metabolism ; Sucrose/metabolism
Chemical Substances	Receptors, N-Methyl-D-Aspartate ; Homocysteine (0LVT1QZ0BA) ; Glutamic Acid (3KX376GY7L) ; Sucrose (57-50-1) ; Dizocilpine Maleate (6LR8C1B66Q) ; Glutamate-Ammonia Ligase (EC 6.3.1.2) ; Sodium-Potassium-Exchanging ATPase (EC 7.2.2.13)
Language	English
Publishing date	2021-07-29
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/s10571-021-01132-0
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Zs.A 1727: Show issues

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Article ; Online: Potential Glioprotective Strategies Against Diabetes-Induced Brain Toxicity.

Sovrani, Vanessa / Bobermin, Larissa Daniele / Schmitz, Izaviany / Leipnitz, Guilhian / Quincozes-Santos, André

Neurotoxicity research

2021 Volume 39, Issue 5, Page(s) 1651–1664

Abstract: Astrocytes are crucial for the maintenance of brain homeostasis by actively participating in the metabolism of glucose, which is the main energy substrate for the central nervous system (CNS), in addition to other supportive functions. More specifically, ...

Abstract	Astrocytes are crucial for the maintenance of brain homeostasis by actively participating in the metabolism of glucose, which is the main energy substrate for the central nervous system (CNS), in addition to other supportive functions. More specifically, astrocytes support neurons through the metabolic coupling of synaptic activity and glucose utilization. As such, diabetes mellitus (DM) and consequent glucose metabolism disorders induce astrocyte damage, affecting CNS functionality. Glioprotective molecules can promote protection by improving glial functions and avoiding toxicity in different pathological conditions, including DM. Therefore, this review discusses specific pathomechanisms associated with DM/glucose metabolism disorder-induced gliotoxicity, namely astrocyte metabolism, redox homeostasis/mitochondrial activity, inflammation, and glial signaling pathways. Studies investigating natural products as potential glioprotective strategies against these deleterious effects of DM/glucose metabolism disorders are also reviewed herein. These products include carotenoids, catechins, isoflavones, lipoic acid, polysaccharides, resveratrol, and sulforaphane.
MeSH term(s)	Animals ; Astrocytes/drug effects ; Astrocytes/metabolism ; Brain/drug effects ; Brain/metabolism ; Diabetes Mellitus/drug therapy ; Diabetes Mellitus/metabolism ; Glucose/antagonists & inhibitors ; Glucose/metabolism ; Humans ; Isoflavones/administration & dosage ; Oxidative Stress/drug effects ; Oxidative Stress/physiology ; Reactive Oxygen Species/antagonists & inhibitors ; Reactive Oxygen Species/metabolism ; Resveratrol/administration & dosage ; Thioctic Acid/administration & dosage
Chemical Substances	Isoflavones ; Reactive Oxygen Species ; Thioctic Acid (73Y7P0K73Y) ; Glucose (IY9XDZ35W2) ; Resveratrol (Q369O8926L)
Language	English
Publishing date	2021-07-14
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2036826-4
ISSN	1476-3524 ; 1029-8428
ISSN (online)	1476-3524
ISSN	1029-8428
DOI	10.1007/s12640-021-00393-3
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