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Article ; Online: α-Synuclein Interactions in Mitochondria-ER Contacts: A Possible Role in Parkinson's Disease.

Erustes, Adolfo Garcia / Guarache, Gabriel Cicolin / Guedes, Erika da Cruz / Leão, Anderson Henrique França Figueredo / Pereira, Gustavo José da Silva / Smaili, Soraya Soubhi

Contact (Thousand Oaks (Ventura County, Calif.))

2022 Volume 5, Page(s) 25152564221119347

Abstract: Endoplasmic reticulum-mitochondria contact sites regulate various biological processes, such as mitochondrial dynamics, calcium homeostasis, autophagy and lipid metabolism. Notably, dysfunctions in these contact sites are closely related to ... ...

Abstract	Endoplasmic reticulum-mitochondria contact sites regulate various biological processes, such as mitochondrial dynamics, calcium homeostasis, autophagy and lipid metabolism. Notably, dysfunctions in these contact sites are closely related to neurodegenerative diseases, including Parkinson's disease, Alzheimer's disease and amyotrophic lateral sclerosis. However, details about the role of endoplasmic reticulum-mitochondria contact sites in neurodegenerative diseases remain unknown. In Parkinson's disease, interactions between α-synuclein in the contact sites and components of tether complexes that connect organelles can lead to various dysfunctions, especially with regards to calcium homeostasis. This review will summarize the main tether complexes present in endoplasmic reticulum-mitochondria contact sites, and their roles in calcium homeostasis and trafficking. We will discuss the impact of α-synuclein accumulation, its interaction with tethering complex components and the implications in Parkinson's disease pathology.
Language	English
Publishing date	2022-08-07
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2964312-0
ISSN	2515-2564 ; 2515-2564
ISSN (online)	2515-2564
ISSN	2515-2564
DOI	10.1177/25152564221119347
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Article ; Online: NAADP-Evoked Ca

Pereira, Cássia Arruda de Souza / Medaglia, Natalia de Castro / Ureshino, Rodrigo Portes / Bincoletto, Claudia / Antonioli, Manuela / Fimia, Gian Maria / Piacentini, Mauro / Pereira, Gustavo José da Silva / Erustes, Adolfo Garcia / Smaili, Soraya Soubhi

International journal of molecular sciences

2023 Volume 24, Issue 6

Abstract: Huntington's disease (HD) is a progressive neurodegenerative disease characterized by mutations in the huntingtin gene (mHtt), causing an unstable repeat of the CAG trinucleotide, leading to abnormal long repeats of polyglutamine (poly-Q) in the N- ... ...

Abstract	Huntington's disease (HD) is a progressive neurodegenerative disease characterized by mutations in the huntingtin gene (mHtt), causing an unstable repeat of the CAG trinucleotide, leading to abnormal long repeats of polyglutamine (poly-Q) in the N-terminal region of the huntingtin, which form abnormal conformations and aggregates. Alterations in Ca
MeSH term(s)	Mice ; Animals ; Calcium Channels/metabolism ; Astrocytes/metabolism ; Neurodegenerative Diseases/metabolism ; NADP/metabolism ; Lysosomes/metabolism ; Autophagy ; Calcium/metabolism ; Huntingtin Protein/genetics ; Huntingtin Protein/metabolism
Chemical Substances	Calcium Channels ; NAADP (5502-96-5) ; NADP (53-59-8) ; Calcium (SY7Q814VUP) ; Huntingtin Protein
Language	English
Publishing date	2023-03-15
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/ijms24065593
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Article: Lack of Autophagy Induction by Lithium Decreases Neuroprotective Effects in the Striatum of Aged Rats.

Costa, Angelica Jardim / Erustes, Adolfo Garcia / Sinigaglia, Rita / Girardi, Carlos Eduardo Neves / Pereira, Gustavo José da Silva / Ureshino, Rodrigo Portes / Smaili, Soraya Soubhi

Pharmaceutics

2021 Volume 13, Issue 2

Abstract: The pharmacological modulation of autophagy is considered a promising neuroprotective strategy. While it has been postulated that lithium regulates this cellular process, the age-related effects have not been fully elucidated. Here, we evaluated lithium- ... ...

Abstract	The pharmacological modulation of autophagy is considered a promising neuroprotective strategy. While it has been postulated that lithium regulates this cellular process, the age-related effects have not been fully elucidated. Here, we evaluated lithium-mediated neuroprotective effects in young and aged striatum. After determining the optimal experimental conditions for inducing autophagy in loco with lithium carbonate (Li
Language	English
Publishing date	2021-01-21
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527217-2
ISSN	1999-4923
ISSN	1999-4923
DOI	10.3390/pharmaceutics13020135
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Article: Activation of estrogen receptor ESR1 and ESR2 induces proliferation of the human testicular embryonal carcinoma NT2/D1 cells

Macheroni, Carla / Gameiro Lucas, Thaís Fabiana / Souza, Deborah Simão / Vicente, Carolina Meloni / Pereira, Gustavo José da Silva / Junior, Itabajara da Silva Vaz / Juliano, Maria Aparecida / Porto, Catarina Segreti

Molecular and cellular endocrinology. 2022 Aug. 20, v. 554

2022

Abstract: The aims of the present study were to investigate the expression of the classic estrogen receptors ESR1 and ESR2, the splicing variant ESR1-36 and GPER in human testicular embryonal carcinoma NT2/D1 cells, and the effects of the activation of the ESR1 ... ...

Abstract	The aims of the present study were to investigate the expression of the classic estrogen receptors ESR1 and ESR2, the splicing variant ESR1-36 and GPER in human testicular embryonal carcinoma NT2/D1 cells, and the effects of the activation of the ESR1 and ESR2 on cell proliferation. Immunostaining of ESR1, ESR2, and GPER were predominantly found in the nuclei, and less abundant in the cytoplasm. ESR1-36 isoform was predominantly expressed in the perinuclear region and cytoplasm, and some weakly immunostained in the nuclei. In nonstimulated NT2/D1 cells (control), proteins of the cell cycle CCND1, CCND2, CCNE1 and CDKN1B are present. Activation of ESR1 and ESR2 increases, respectively, CCND2 and CCNE1 expression, but not CCND1. Activation of ESR2 also mediates upregulation of the cell cycle inhibitor CDKN1B. This protein co-immunoprecipitated with CCND2. Also, E2 induces an increase in the number and viability of the NT2/D1 cells. These effects are blocked by simultaneous pretreatment with ESR1-and ESR2-selective antagonists, confirming that both estrogen receptors regulate NT2/D1 cell proliferation. In addition, E2 increases SRC phosphorylation, and SRC mediates cell proliferation. Our study provides novel insights into the signatures and molecular mechanisms of estrogen receptor in NT2/D1 cells.
Keywords	carcinoma ; cell cycle ; cell proliferation ; cytoplasm ; estrogen receptors ; estrogens ; humans ; phosphorylation ; testes ; viability
Language	English
Dates of publication	2022-0820
Publishing place	Elsevier B.V.
Document type	Article
ZDB-ID	187438-x
ISSN	1872-8057 ; 0303-7207
ISSN (online)	1872-8057
ISSN	0303-7207
DOI	10.1016/j.mce.2022.111708
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Activation of estrogen receptor ESR1 and ESR2 induces proliferation of the human testicular embryonal carcinoma NT2/D1 cells.

Molecular and cellular endocrinology

2022 Volume 554, Page(s) 111708

Abstract	The aims of the present study were to investigate the expression of the classic estrogen receptors ESR1 and ESR2, the splicing variant ESR1-36 and GPER in human testicular embryonal carcinoma NT2/D1 cells, and the effects of the activation of the ESR1 and ESR2 on cell proliferation. Immunostaining of ESR1, ESR2, and GPER were predominantly found in the nuclei, and less abundant in the cytoplasm. ESR1-36 isoform was predominantly expressed in the perinuclear region and cytoplasm, and some weakly immunostained in the nuclei. In nonstimulated NT2/D1 cells (control), proteins of the cell cycle CCND1, CCND2, CCNE1 and CDKN1B are present. Activation of ESR1 and ESR2 increases, respectively, CCND2 and CCNE1 expression, but not CCND1. Activation of ESR2 also mediates upregulation of the cell cycle inhibitor CDKN1B. This protein co-immunoprecipitated with CCND2. Also, E2 induces an increase in the number and viability of the NT2/D1 cells. These effects are blocked by simultaneous pretreatment with ESR1-and ESR2-selective antagonists, confirming that both estrogen receptors regulate NT2/D1 cell proliferation. In addition, E2 increases SRC phosphorylation, and SRC mediates cell proliferation. Our study provides novel insights into the signatures and molecular mechanisms of estrogen receptor in NT2/D1 cells.
MeSH term(s)	Carcinoma, Embryonal ; Cell Proliferation ; Estrogen Receptor alpha/metabolism ; Estrogen Receptor beta/genetics ; Estrogen Receptor beta/metabolism ; Humans ; Phosphorylation ; Receptors, Estrogen/metabolism
Chemical Substances	ESR1 protein, human ; ESR2 protein, human ; Estrogen Receptor alpha ; Estrogen Receptor beta ; Receptors, Estrogen
Language	English
Publishing date	2022-07-02
Publishing country	Ireland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	187438-x
ISSN	1872-8057 ; 0303-7207
ISSN (online)	1872-8057
ISSN	0303-7207
DOI	10.1016/j.mce.2022.111708
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ab Jg. 2022: Lesesaal (EG)

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Article ; Online: Effects of ICI 182,780, an ERα and ERβ antagonist, and G-1, a GPER agonist, on autophagy in breast cancer cells.

Muler, Mari Luminosa / Antunes, Fernanda / Guarache, Gabriel Cicolin / Oliveira, Rafaela Brito / Ureshino, Rodrigo Portes / Bincoletto, Claudia / Pereira, Gustavo José da Silva / Smaili, Soraya Soubhi

Einstein (Sao Paulo, Brazil)

2020 Volume 18, Page(s) eAO4560

Abstract: Objective: To investigate if ICI 182,780 (fulvestrant), a selective estrogen receptor alpha/beta (ERα/ERβ) antagonist, and G-1, a selective G-protein-coupled receptor (GPER) agonist, can potentially induce autophagy in breast cancer cell lines MCF-7 and ...

Abstract	Objective: To investigate if ICI 182,780 (fulvestrant), a selective estrogen receptor alpha/beta (ERα/ERβ) antagonist, and G-1, a selective G-protein-coupled receptor (GPER) agonist, can potentially induce autophagy in breast cancer cell lines MCF-7 and SKBr3, and how G-1 affects cell viability. Methods: Cell viability in MCF-7 and SKBr3 cells was assessed by the MTT assay. To investigate the autophagy flux, MCF-7 cells were transfected with GFP-LC3, a marker of autophagosomes, and analyzed by real-time fluorescence microscopy. MCF-7 and SKBr3 cells were incubated with acridine orange for staining of acidic vesicular organelles and analyzed by flow cytometry as an indicator of autophagy. Results: Regarding cell viability in MCF-7 cells, ICI 182,780 and rapamycin, after 48 hours, led to decreased cell proliferation whereas G-1 did not change viability over the same period. The data showed that neither ICI 182,780 nor G-1 led to increased GFP-LC3 puncta in MCF-7 cells over the 4-hour observation period. The cytometry assay showed that ICI 182,780 led to a higher number of acidic vesicular organelles in MCF-7 cells. G-1, in turn, did not have this effect in any of the cell lines. In contrast, ICI 182,780 and G-1 did not decrease cell viability of SKBr3 cells or induce formation of acidic vesicular organelles, which corresponds to the final step of the autophagy process in this cell line. Conclusion: The effect of ICI 182,780 on increasing acidic vesicular organelles in estrogen receptor-positive breast cancer cells appears to be associated with its inhibitory effect on estrogen receptors, and GPER does notseem to be involved. Understanding these mechanisms may guide further investigations of these receptors' involvement in cellular processes of breast cancer resistance.
MeSH term(s)	Analysis of Variance ; Autophagy/drug effects ; Blotting, Western ; Breast Neoplasms/drug therapy ; Breast Neoplasms/pathology ; Cell Proliferation/drug effects ; Cell Survival/drug effects ; Estrogen Receptor Antagonists/pharmacology ; Estrogen Receptor alpha/antagonists & inhibitors ; Estrogen Receptor beta/antagonists & inhibitors ; Female ; Flow Cytometry/methods ; Fulvestrant/pharmacology ; Humans ; MCF-7 Cells ; Receptors, G-Protein-Coupled/agonists ; Receptors, G-Protein-Coupled/analysis ; Reproducibility of Results ; Sirolimus/pharmacology ; Time Factors ; Transfection/methods
Chemical Substances	Estrogen Receptor Antagonists ; Estrogen Receptor alpha ; Estrogen Receptor beta ; Receptors, G-Protein-Coupled ; Fulvestrant (22X328QOC4) ; Sirolimus (W36ZG6FT64)
Language	Portuguese
Publishing date	2020-04-22
Publishing country	Brazil
Document type	Evaluation Study ; Journal Article
ZDB-ID	2418293-X
ISSN	2317-6385 ; 1679-4508
ISSN (online)	2317-6385
ISSN	1679-4508
DOI	10.31744/einstein_journal/2020AO4560
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Article ; Online: Membrane estrogen receptor ERα activation improves tau clearance via autophagy induction in a tauopathy cell model.

Costa, Angelica Jardim / Oliveira, Rafaela Brito / Wachilewski, Patrícia / Nishino, Michelle Sayuri / Bassani, Taysa Bervian / Stilhano, Roberta Sessa / Cerutti, Janete Maria / Nozima, Bruno / Porto, Catarina Segreti / Pereira, Gustavo Jose da Silva / Ramirez, Ana Lopez / Smaili, Soraya Soubhi / Ureshino, Rodrigo Portes

Brain research

2022 Volume 1795, Page(s) 148079

Abstract: Alzheimer's disease (AD) is the most prevalent aging-associated neurodegenerative disease, with a higher incidence in women than men. There is evidence that sex hormone replacement therapy, particularly estrogen, reduces memory loss in menopausal women. ... ...

Abstract	Alzheimer's disease (AD) is the most prevalent aging-associated neurodegenerative disease, with a higher incidence in women than men. There is evidence that sex hormone replacement therapy, particularly estrogen, reduces memory loss in menopausal women. Neurofibrillary tangles are associated with tau protein aggregation, a characteristic of AD and other tauopathies. In this sense, autophagy is a promising cellular process to remove these protein aggregates. This study evaluated the autophagy mechanisms involved in neuroprotection induced by 17β-estradiol (E2) in a Tet-On inducible expression tauopathy cell model (EGFP-tau WT or with the P301L mutation, 0N4R isoform). The results indicated that 17β-estradiol induces autophagy by activating AMPK in a concentration-dependent manner, independent of mTOR signals. The estrogen receptor α (ERα) agonist, PPT, also induced autophagy, while the ERα antagonist, MPP, substantially attenuated the 17β-estradiol-mediated autophagy induction. Notably, 17β-estradiol increased LC3-II levels and phosphorylated and total tau protein clearance in the EGFP-tau WT cell line but not in EGPF-tau P301L. Similar results were observed with E2-BSA, a plasma membrane-impermeable estrogen, suggesting membrane ERα involvement in non-genomic estrogenic pathway activation. Furthermore, 17β-estradiol-induced autophagy led to EGFP-tau protein clearance. These results demonstrate that modulating autophagy via the estrogenic pathway may represent a new therapeutic target for treating AD.
MeSH term(s)	AMP-Activated Protein Kinases ; Alzheimer Disease ; Autophagy ; Estradiol/pharmacology ; Estrogen Receptor alpha/metabolism ; Estrogens/pharmacology ; Female ; Humans ; Male ; Neurodegenerative Diseases ; Protein Aggregates ; Receptors, Estrogen ; TOR Serine-Threonine Kinases ; Tauopathies ; tau Proteins/metabolism
Chemical Substances	Estrogen Receptor alpha ; Estrogens ; Protein Aggregates ; Receptors, Estrogen ; tau Proteins ; Estradiol (4TI98Z838E) ; TOR Serine-Threonine Kinases (EC 2.7.11.1) ; AMP-Activated Protein Kinases (EC 2.7.11.31)
Language	English
Publishing date	2022-09-08
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1200-2
ISSN	1872-6240 ; 0006-8993
ISSN (online)	1872-6240
ISSN	0006-8993
DOI	10.1016/j.brainres.2022.148079
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Zs.A 161: Show issues

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Article ; Online: Effects of Aging in the Striatum and Substantia Nigra of a Parkinson's Disease Animal Model.

Ureshino, Rodrigo Portes / Costa, Angelica Jardim / Erustes, Adolfo Garcia / Pereira, Gustavo José da Silva / Sinigaglia-Coimbra, Rita / Smaili, Soraya Soubhi

Toxicologic pathology

2018 Volume 46, Issue 3, Page(s) 348–358

Abstract: Aging is a multifactorial process associated with functional deficits, and the brain is more prone to developing chronic degenerative diseases such as Parkinson's disease. Several groups have tried to correlate the age-related ultrastructural alterations ...

Abstract	Aging is a multifactorial process associated with functional deficits, and the brain is more prone to developing chronic degenerative diseases such as Parkinson's disease. Several groups have tried to correlate the age-related ultrastructural alterations to the neurodegeneration process using in vivo pharmacological models, but due to the limitations of the animal models, particularly in aged animals, the results are difficult to interpret. In this work, we investigated neurodegeneration induced by rotenone, as a pharmacological model of Parkinson's disease, in both young and aged Wistar rats. We assessed animal mobility, tyrosine hydroxylase staining in the substantia nigra pars compacta (SNpc), and TdT-mediated dUTP-biotin nick end labeling-positive nuclei and reactive oxygen species production in the striatum. Interestingly, the mobility impairment, dopaminergic neuron loss, and elevated number of apoptotic nuclei in the striatum of aged control rats were similar to young rotenone-treated animals. Moreover, we observed many ultrastructural alterations, such as swollen mitochondria in the striatum, and massive lipofuscin deposits in the SNpc of the aged rotenone-treated animals. We conclude that the rotenone model can be employed to explore age-related alterations in the ontogeny that can increase vulnerability in the striatum and SNpc, which may contribute to Parkinson's disease pathogenesis.
MeSH term(s)	Aging/pathology ; Animals ; Corpus Striatum/pathology ; Parkinsonian Disorders/pathology ; Rats ; Rats, Wistar ; Rotenone/toxicity ; Substantia Nigra/pathology ; Uncoupling Agents/toxicity
Chemical Substances	Uncoupling Agents ; Rotenone (03L9OT429T)
Language	English
Publishing date	2018-04-22
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	841009-4
ISSN	1533-1601 ; 0192-6233
ISSN (online)	1533-1601
ISSN	0192-6233
DOI	10.1177/0192623318767065
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Zs.A 1975: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: The Interplay between Ca

Ureshino, Rodrigo Portes / Erustes, Adolfo Garcia / Bassani, Taysa Bervian / Wachilewski, Patrícia / Guarache, Gabriel Cicolin / Nascimento, Ana Carolina / Costa, Angelica Jardim / Smaili, Soraya Soubhi / Pereira, Gustavo José da Silva

International journal of molecular sciences

2019 Volume 20, Issue 23

Abstract: ... Calcium ( ... ...

Abstract	Calcium (Ca
MeSH term(s)	Animals ; Autophagy ; Calcium Channels/metabolism ; Calcium Signaling ; Humans ; Inositol 1,4,5-Trisphosphate Receptors/metabolism ; Neurodegenerative Diseases/metabolism ; Ryanodine Receptor Calcium Release Channel/metabolism
Chemical Substances	Calcium Channels ; Inositol 1,4,5-Trisphosphate Receptors ; Ryanodine Receptor Calcium Release Channel
Language	English
Publishing date	2019-11-28
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/ijms20236004
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Article ; Online: Pharmacological Modulators of Autophagy as a Potential Strategy for the Treatment of COVID-19.

Pereira, Gustavo José da Silva / Leão, Anderson Henrique França Figueredo / Erustes, Adolfo Garcia / Morais, Ingrid Beatriz de Melo / Vrechi, Talita Aparecida de Moraes / Zamarioli, Lucas Dos Santos / Pereira, Cássia Arruda Souza / Marchioro, Laís de Oliveira / Sperandio, Letícia Paulino / Lins, Ísis Valeska Freire / Piacentini, Mauro / Fimia, Gian Maria / Reckziegel, Patrícia / Smaili, Soraya Soubhi / Bincoletto, Claudia

International journal of molecular sciences

2021 Volume 22, Issue 8

Abstract: The family of coronaviruses (CoVs) uses the autophagy machinery of host cells to promote their growth and replication; thus, this process stands out as a potential target to combat COVID-19. Considering the different roles of autophagy during viral ... ...

Abstract	The family of coronaviruses (CoVs) uses the autophagy machinery of host cells to promote their growth and replication; thus, this process stands out as a potential target to combat COVID-19. Considering the different roles of autophagy during viral infection, including SARS-CoV-2 infection, in this review, we discuss several clinically used drugs that have effects at different stages of autophagy. Among them, we mention (1) lysosomotropic agents, which can prevent CoVs infection by alkalinizing the acid pH in the endolysosomal system, such as chloroquine and hydroxychloroquine, azithromycin, artemisinins, two-pore channel modulators and imatinib; (2) protease inhibitors that can inhibit the proteolytic cleavage of the spike CoVs protein, which is necessary for viral entry into host cells, such as camostat mesylate, lopinavir, umifenovir and teicoplanin and (3) modulators of PI3K/AKT/mTOR signaling pathways, such as rapamycin, heparin, glucocorticoids, angiotensin-converting enzyme inhibitors (IECAs) and cannabidiol. Thus, this review aims to highlight and discuss autophagy-related drugs for COVID-19, from in vitro to in vivo studies. We identified specific compounds that may modulate autophagy and exhibit antiviral properties. We hope that research initiatives and efforts will identify novel or "off-label" drugs that can be used to effectively treat patients infected with SARS-CoV-2, reducing the risk of mortality.
MeSH term(s)	Autophagy/drug effects ; Humans ; Molecular Targeted Therapy ; SARS-CoV-2/drug effects ; SARS-CoV-2/physiology ; Signal Transduction ; Virus Replication/drug effects ; Virus Replication/physiology ; COVID-19 Drug Treatment
Language	English
Publishing date	2021-04-15
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/ijms22084067
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