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Article: Editorial: Autophagy in the central nervous system: Focus on neurons, glia and neuron-glia interactions.

Jimenez-Sanchez, Maria / Pampliega, Olatz / Soukup, Sandra-Fausia

Frontiers in cell and developmental biology

2022 Volume 10, Page(s) 1036587

Language	English
Publishing date	2022-10-12
Publishing country	Switzerland
Document type	Editorial
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2022.1036587
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Article ; Online: Autophagy in Astrocytes and its Implications in Neurodegeneration.

Sung, Katherine / Jimenez-Sanchez, Maria

Journal of molecular biology

2020 Volume 432, Issue 8, Page(s) 2605–2621

Abstract: Autophagy is a major degradation pathway where double-membrane vesicles called autophagosomes deliver cytoplasmic content to the lysosome. Increasing evidence suggests that autophagy dysfunction contributes to the pathogenesis of neurodegenerative ... ...

Abstract	Autophagy is a major degradation pathway where double-membrane vesicles called autophagosomes deliver cytoplasmic content to the lysosome. Increasing evidence suggests that autophagy dysfunction contributes to the pathogenesis of neurodegenerative diseases. In addition, misfolded proteins that accumulate in these diseases and constitute a common pathological hallmark are substrates for autophagic degradation. Astrocytes, a major type of glial cells, are emerging as a critical component in most neurodegenerative diseases. This review will summarize the recent efforts to investigate the role that autophagy plays in astrocytes in the context of neurodegenerative diseases. While the field has mostly focused on the implications of autophagy in neurons, autophagy may also be involved in the clearance of disease-related proteins in astrocytes as well as in maintaining astrocyte function, which could impact the cell autonomous and non-cell autonomous contribution of astrocytes to neurodegeneration.
MeSH term(s)	Animals ; Astrocytes/pathology ; Autophagosomes/physiology ; Autophagy ; Humans ; Neurodegenerative Diseases/pathology
Language	English
Publishing date	2020-01-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	80229-3
ISSN	1089-8638 ; 0022-2836
ISSN (online)	1089-8638
ISSN	0022-2836
DOI	10.1016/j.jmb.2019.12.041
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Zs.A 867: Show issues

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Article ; Online: Microglial cytokines poison neuronal autophagy via CCR5, a druggable target.

Festa, Beatrice Paola / Siddiqi, Farah H / Jimenez-Sanchez, Maria / Rubinsztein, David C

Autophagy

2023 Volume 20, Issue 4, Page(s) 949–951

Abstract: In the prodromal phase of neurodegenerative diseases, microglia switch to an activated state resulting in increased secretion of pro-inflammatory factors. We reported that C - C chemokine ligand 3 (CCL3), C - C chemokine ligand 4 (CCL4) and C - C ... ...

Abstract	In the prodromal phase of neurodegenerative diseases, microglia switch to an activated state resulting in increased secretion of pro-inflammatory factors. We reported that C - C chemokine ligand 3 (CCL3), C - C chemokine ligand 4 (CCL4) and C - C chemokine ligand 5 (CCL5) contained in the secretome of activated microglia inhibit neuronal autophagy via a non-cell autonomous mechanism. These chemokines bind and activate neuronal C - C chemokine receptor type 5 (CCR5), which, in turn, promotes phosphoinositide 3-kinase (PI3K) - protein kinase B (PKB, or AKT) - mammalian target of rapamycin complex 1 (mTORC1) pathway activation, which inhibits autophagy, thus causing the accumulation of aggregate-prone proteins in the cytoplasm of neurons. The levels of CCR5 and its chemokine ligands are increased in the brains of pre-manifesting Huntington disease (HD) and tauopathy mouse models. CCR5 accumulation might be due to a self-amplifying mechanism, since CCR5 is a substrate of autophagy and CCL5-CCR5-mediated autophagy inhibition impairs CCR5 degradation. Furthermore, pharmacological, or genetic inhibition of CCR5 rescues mTORC1-autophagy dysfunction and improves neurodegeneration in HD and tauopathy mouse models, suggesting that CCR5 hyperactivation is a pathogenic signal driving the progression of these diseases.
MeSH term(s)	Animals ; Humans ; Mice ; Autophagy/drug effects ; Autophagy/physiology ; Cytokines/metabolism ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Microglia/metabolism ; Microglia/drug effects ; Molecular Targeted Therapy ; Neurons/metabolism ; Receptors, CCR5/metabolism ; Signal Transduction
Chemical Substances	Cytokines ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1) ; Receptors, CCR5 ; CCR5 protein, mouse
Language	English
Publishing date	2023-06-26
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2023.2221921
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Article: The impact of ultrasound, micro-oxygenation and oak wood type on the phenolic and volatile composition of a Tempranillo red wine

Jiménez-Sánchez, María / Castro, Remedios / Rodríguez-Dodero, M. Carmen / Durán-Guerrero, Enrique

Lebensmittel-Wissenschaft + Technologie. 2022 June 15, v. 163

2022

Abstract: The accelerated ageing of a Tempranillo red wine has been studied at pilot scale through the combined application of ultrasound, micro-oxygenation and different oak wood type chips (American, French and Spanish). The phenolic and volatile content of the ... ...

Abstract	The accelerated ageing of a Tempranillo red wine has been studied at pilot scale through the combined application of ultrasound, micro-oxygenation and different oak wood type chips (American, French and Spanish). The phenolic and volatile content of the aged samples and their sensory profiles have been determined. The wine samples that had been aged using micro-oxygenation, French or American oak chips, and ultrasound revealed to be similar in terms of polyphenols to those wines that had been aged without implementing this last accelerating technique. Ageing time, with a high extraction kinetics, was the most significant variable with regard to their polyphenol content. In terms of volatiles, Spanish and French oak wood wine samples showed a similar behaviour closely associated to ageing time, while American oak wood achieved a rather low enrichment in volatile constituents, resulting in a poor sensory profile of the final wines, which was particularly poor in the case of ultrasound aged wines.
Keywords	polyphenols ; red wines ; sensory evaluation ; ultrasonics ; volatile compounds ; wood
Language	English
Dates of publication	2022-0615
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	241369-3
ISSN	0460-1173 ; 0023-6438
ISSN	0460-1173 ; 0023-6438
DOI	10.1016/j.lwt.2022.113618
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Microglial-to-neuronal CCR5 signaling regulates autophagy in neurodegeneration.

Festa, Beatrice Paola / Siddiqi, Farah H / Jimenez-Sanchez, Maria / Won, Hyeran / Rob, Matea / Djajadikerta, Alvin / Stamatakou, Eleanna / Rubinsztein, David C

Neuron

2023 Volume 111, Issue 13, Page(s) 2021–2037.e12

Abstract: In neurodegenerative diseases, microglia switch to an activated state, which results in excessive secretion of pro-inflammatory factors. Our work aims to investigate how this paracrine signaling affects neuronal function. Here, we show that activated ... ...

Abstract	In neurodegenerative diseases, microglia switch to an activated state, which results in excessive secretion of pro-inflammatory factors. Our work aims to investigate how this paracrine signaling affects neuronal function. Here, we show that activated microglia mediate non-cell-autonomous inhibition of neuronal autophagy, a degradative pathway critical for the removal of toxic, aggregate-prone proteins accumulating in neurodegenerative diseases. We found that the microglial-derived CCL-3/-4/-5 bind and activate neuronal CCR5, which in turn promotes mTORC1 activation and disrupts autophagy and aggregate-prone protein clearance. CCR5 and its cognate chemokines are upregulated in the brains of pre-manifesting mouse models for Huntington's disease (HD) and tauopathy, suggesting a pathological role of this microglia-neuronal axis in the early phases of these diseases. CCR5 upregulation is self-sustaining, as CCL5-CCR5 autophagy inhibition impairs CCR5 degradation itself. Finally, pharmacological or genetic inhibition of CCR5 rescues mTORC1 hyperactivation and autophagy dysfunction, which ameliorates HD and tau pathologies in mouse models.
MeSH term(s)	Mice ; Animals ; Microglia/metabolism ; Signal Transduction ; Autophagy ; Neurodegenerative Diseases/metabolism ; Proteins/metabolism ; Huntington Disease/metabolism ; Mechanistic Target of Rapamycin Complex 1/metabolism
Chemical Substances	Proteins ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1)
Language	English
Publishing date	2023-04-26
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	808167-0
ISSN	1097-4199 ; 0896-6273
ISSN (online)	1097-4199
ISSN	0896-6273
DOI	10.1016/j.neuron.2023.04.006
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Zs.A 2496: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Proteomics of the astrocyte secretome reveals changes in their response to soluble oligomeric Aβ.

Matafora, Vittoria / Gorb, Alena / Yang, Fangjia / Noble, Wendy / Bachi, Angela / Perez-Nievas, Beatriz Gomez / Jimenez-Sanchez, Maria

Journal of neurochemistry

2023 Volume 166, Issue 2, Page(s) 346–366

Abstract: Astrocytes associate with amyloid plaques in Alzheimer's disease (AD). Astrocytes react to changes in the brain environment, including increasing concentrations of amyloid-β (Aβ). However, the precise response of astrocytes to soluble small Aβ oligomers ... ...

Abstract	Astrocytes associate with amyloid plaques in Alzheimer's disease (AD). Astrocytes react to changes in the brain environment, including increasing concentrations of amyloid-β (Aβ). However, the precise response of astrocytes to soluble small Aβ oligomers at concentrations similar to those present in the human brain has not been addressed. In this study, we exposed astrocytes to media from neurons that express the human amyloid precursor protein (APP) transgene with the double Swedish mutation (APPSwe), and which contains APP-derived fragments, including soluble human Aβ oligomers. We then used proteomics to investigate changes in the astrocyte secretome. Our data show dysregulated secretion of astrocytic proteins involved in the extracellular matrix and cytoskeletal organization and increase secretion of proteins involved in oxidative stress responses and those with chaperone activity. Several of these proteins have been identified in previous transcriptomic and proteomic studies using brain tissue from human AD and cerebrospinal fluid (CSF). Our work highlights the relevance of studying astrocyte secretion to understand the brain response to AD pathology and the potential use of these proteins as biomarkers for the disease.
MeSH term(s)	Humans ; Astrocytes/metabolism ; Proteomics ; Secretome ; Amyloid beta-Peptides/metabolism ; Alzheimer Disease/metabolism ; Amyloid beta-Protein Precursor/metabolism
Chemical Substances	Amyloid beta-Peptides ; Amyloid beta-Protein Precursor
Language	English
Publishing date	2023-06-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80158-6
ISSN	1471-4159 ; 0022-3042 ; 1474-1644
ISSN (online)	1471-4159
ISSN	0022-3042 ; 1474-1644
DOI	10.1111/jnc.15875
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Article ; Online: Astrocyte adaptation in Alzheimer's disease: a focus on astrocytic P2X7R.

Beltran-Lobo, Paula / Reid, Matthew J / Jimenez-Sanchez, Maria / Verkhratsky, Alexei / Perez-Nievas, Beatriz G / Noble, Wendy

Essays in biochemistry

2023 Volume 67, Issue 1, Page(s) 119–130

Abstract: Astrocytes are key homeostatic and defensive cells of the central nervous system (CNS). They undertake numerous functions during development and in adulthood to support and protect the brain through finely regulated communication with other cellular ... ...

Abstract	Astrocytes are key homeostatic and defensive cells of the central nervous system (CNS). They undertake numerous functions during development and in adulthood to support and protect the brain through finely regulated communication with other cellular elements of the nervous tissue. In Alzheimer's disease (AD), astrocytes undergo heterogeneous morphological, molecular and functional alterations represented by reactive remodelling, asthenia and loss of function. Reactive astrocytes closely associate with amyloid β (Aβ) plaques and neurofibrillary tangles in advanced AD. The specific contribution of astrocytes to AD could potentially evolve along the disease process and includes alterations in their signalling, interactions with pathological protein aggregates, metabolic and synaptic impairments. In this review, we focus on the purinergic receptor, P2X7R, and discuss the evidence that P2X7R activation contributes to altered astrocyte functions in AD. Expression of P2X7R is increased in AD brain relative to non-demented controls, and animal studies have shown that P2X7R antagonism improves cognitive and synaptic impairments in models of amyloidosis and tauopathy. While P2X7R activation can induce inflammatory signalling pathways, particularly in microglia, we focus here specifically on the contributions of astrocytic P2X7R to synaptic changes and protein aggregate clearance in AD, highlighting cell-specific roles of this purinoceptor activation that could be targeted to slow disease progression.
MeSH term(s)	Animals ; Alzheimer Disease/metabolism ; Astrocytes/metabolism ; Astrocytes/pathology ; Amyloid beta-Peptides/metabolism ; Brain/metabolism ; Signal Transduction
Chemical Substances	Amyloid beta-Peptides
Language	English
Publishing date	2023-01-18
Publishing country	England
Document type	Review ; Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1744-1358 ; 0071-1365
ISSN (online)	1744-1358
ISSN	0071-1365
DOI	10.1042/EBC20220079
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Article ; Online: Men and women differ in their perception of gender bias in research institutions.

García-González, Judit / Forcén, Patricia / Jimenez-Sanchez, Maria

PloS one

2019 Volume 14, Issue 12, Page(s) e0225763

Abstract: There is extensive evidence of gender inequality in research leading to insufficient representation of women in leadership positions. Numbers revealing a gender gap in research are periodically reported by national and international institutions but data ...

Abstract	There is extensive evidence of gender inequality in research leading to insufficient representation of women in leadership positions. Numbers revealing a gender gap in research are periodically reported by national and international institutions but data on perceptions of gender equality within the research community are scarce. In the present study, a questionnaire based on the British Athena Survey of Science, Engineering and Technology (ASSET 2016) was distributed among researchers working in Spain. Consistent with the original UK-based study, women in research perceived a greater degree of gender inequality than men. This difference was consistent from junior to senior positions, within public and private universities as well as research centres, and across all research disciplines. When responses were compared with the existing UK-based questionnaire, researchers in Spain felt that women and men are treated more equally in the workplace, yet they perceived their home departments to be less supportive regarding matters of gender equality. The results of this study provide clear evidence that men and women do not share the same perceptions of gender equality in science and that their differing perceptions are relatively consistent across two major European countries. The fact that men occupy the majority of senior positions while not perceiving the same inequality as women do, may be critical when it comes to ensuring the fair ascent of women to senior positions in an academic system. These data encourage the implementation of measures to ensure that both men and women are aware of gender biases in research.
MeSH term(s)	Academies and Institutes ; Adult ; Aged ; Female ; Humans ; Male ; Middle Aged ; Perception ; Sexism ; Spain ; United Kingdom ; Young Adult
Language	English
Publishing date	2019-12-05
Publishing country	United States
Document type	Journal Article
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0225763
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Article: A Microstructure Insight of MTA Repair HP of Rapid Setting Capacity and Bioactive Response.

Jiménez-Sánchez, María Carmen / Segura-Egea, Juan José / Díaz-Cuenca, Aránzazu

Materials (Basel, Switzerland)

2020 Volume 13, Issue 7

Abstract: Mineral trioxide aggregate (MTA) is considered a bioactive endodontic material, which promotes natural mineralization at the material-tooth tissue interface. MTA Repair HP stands out because of the short setting time and the quick and effective bioactive ...

Abstract	Mineral trioxide aggregate (MTA) is considered a bioactive endodontic material, which promotes natural mineralization at the material-tooth tissue interface. MTA Repair HP stands out because of the short setting time and the quick and effective bioactive response in vitro. The bioactivity, depens on material composition and microstructure. This work is devoted to analyze MTA Repair HP microstructural features, of both the powder precursor and set material, to get insights into the material physicochemical parameters-functionality performance relationships. Transmission electron microscopy (TEM), and field emission gun scanning electron microscopy (FEG-SEM) coupled with energy-dispersive X-ray (EDX) analyses were performed. X-ray diffraction (XRD) measurements were carried out at different times to investigate setting process. Bioactivity evaluation in vitro was carried out by soaking the processed cement disk in simulated body fluid (SBF). The presented results point out those MTA Repair HP precursor material characteristics of tricalcium silicate particles of nanometric size and high aspect ratio, which provide an elevated surface area and maximized components dispersion of calcium silicate and very reactive calcium aluminate. The MTA Repair HP precursor powder nanostructure and formulation, allows a hydration process comprising silicate hydrate structures, which are very effective to achieve both fast setting and efficient bioactive response.
Language	English
Publishing date	2020-04-02
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2487261-1
ISSN	1996-1944
ISSN	1996-1944
DOI	10.3390/ma13071641
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Article ; Online: Reactive astrocytes secrete the chaperone HSPB1 to mediate neuroprotection.

Yang, Fangjia / Beltran-Lobo, Paula / Sung, Katherine / Goldrick, Caoimhe / Croft, Cara L / Nishimura, Agnes / Hedges, Erin / Mahiddine, Farah / Troakes, Claire / Golde, Todd E / Perez-Nievas, Beatriz G / Hanger, Diane P / Noble, Wendy / Jimenez-Sanchez, Maria

Science advances

2024 Volume 10, Issue 12, Page(s) eadk9884

Abstract: Molecular chaperones are protective in neurodegenerative diseases by preventing protein misfolding and aggregation, such as extracellular amyloid plaques and intracellular tau neurofibrillary tangles in Alzheimer's disease (AD). In addition, AD is ... ...

Abstract	Molecular chaperones are protective in neurodegenerative diseases by preventing protein misfolding and aggregation, such as extracellular amyloid plaques and intracellular tau neurofibrillary tangles in Alzheimer's disease (AD). In addition, AD is characterized by an increase in astrocyte reactivity. The chaperone HSPB1 has been proposed as a marker for reactive astrocytes; however, its astrocytic functions in neurodegeneration remain to be elucidated. Here, we identify that HSPB1 is secreted from astrocytes to exert non-cell-autonomous protective functions. We show that in human AD brain, HSPB1 levels increase in astrocytes that cluster around amyloid plaques, as well as in the adjacent extracellular space. Moreover, in conditions that mimic an inflammatory reactive response, astrocytes increase HSPB1 secretion. Concomitantly, astrocytes and neurons can uptake astrocyte-secreted HSPB1, which is accompanied by an attenuation of the inflammatory response in reactive astrocytes and reduced pathological tau inclusions. Our findings highlight a protective mechanism in disease conditions that encompasses the secretion of a chaperone typically regarded as intracellular.
MeSH term(s)	Humans ; Astrocytes/metabolism ; tau Proteins/metabolism ; Plaque, Amyloid/pathology ; Neuroprotection ; Molecular Chaperones/metabolism ; Alzheimer Disease/metabolism ; Amyloid beta-Peptides/metabolism ; Heat-Shock Proteins/metabolism
Chemical Substances	tau Proteins ; Molecular Chaperones ; Amyloid beta-Peptides ; HSPB1 protein, human ; Heat-Shock Proteins
Language	English
Publishing date	2024-03-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	2810933-8
ISSN	2375-2548 ; 2375-2548
ISSN (online)	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.adk9884
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