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Article ; Online: Antibody-mediated neutralization of ACBP/DBI has anorexigenic and lipolytic effects.

Sica, Valentina / Martins, Isabelle / Motiño, Omar / Bravo-San Pedro, José M / Kroemer, Guido

Adipocyte

2020 Volume 9, Issue 1, Page(s) 116–119

Abstract: We recently identified acyl coenzyme A-binding protein (ACBP)/diazepam binding inhibitor (DBI) as a novel 'hunger factor': a protein that is upregulated in human or murine obesity and that, if administered to mice, causes hyperphagy, adipogenesis and ... ...

Abstract	We recently identified acyl coenzyme A-binding protein (ACBP)/diazepam binding inhibitor (DBI) as a novel 'hunger factor': a protein that is upregulated in human or murine obesity and that, if administered to mice, causes hyperphagy, adipogenesis and obesity. Conversely, neutralization of ACBP/DBI by systemic injection of neutralizing monoclonal antibodies or autoantibodies produced after auto-immunization against ACBP/DBI has anorexigenic and lipolytic effects. Thus, neutralization of ACBP/DBI results in reduced food intake subsequent to the activation of anorexigenic neurons and the inactivation of orexigenic neurons in the hypothalamus. Moreover, ACBP/DBI neutralization results into enhanced triglyceride lipolysis in white fat, a surge in free fatty acids in the plasma, enhanced incorporation of glycerol-derived carbon atoms into glucose, as well as an increase in β-oxidation, resulting in a net reduction of fat mass. Importantly, ACBP/DBI neutralization also stimulated an increase in autophagy in various organs, suggesting that it might mediate anti-ageing effects.
MeSH term(s)	Animals ; Anorexia/metabolism ; Antibodies/metabolism ; Diazepam Binding Inhibitor/metabolism ; Humans ; Lipolysis
Chemical Substances	Antibodies ; Diazepam Binding Inhibitor
Language	English
Publishing date	2020-03-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ISSN	2162-397X
ISSN (online)	2162-397X
DOI	10.1080/21623945.2020.1736734
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Article ; Online: ER-mitochondria signaling in Parkinson's disease.

Gómez-Suaga, Patricia / Bravo-San Pedro, José M / González-Polo, Rosa A / Fuentes, José M / Niso-Santano, Mireia

Cell death & disease

2018 Volume 9, Issue 3, Page(s) 337

Abstract: Mitochondria form close physical contacts with a specialized domain of the endoplasmic reticulum (ER), known as the mitochondria-associated membrane (MAM). This association constitutes a key signaling hub to regulate several fundamental cellular ... ...

Abstract	Mitochondria form close physical contacts with a specialized domain of the endoplasmic reticulum (ER), known as the mitochondria-associated membrane (MAM). This association constitutes a key signaling hub to regulate several fundamental cellular processes. Alterations in ER-mitochondria signaling have pleiotropic effects on a variety of intracellular events resulting in mitochondrial damage, Ca
MeSH term(s)	Animals ; Endoplasmic Reticulum/genetics ; Endoplasmic Reticulum/metabolism ; Humans ; Mitochondria/genetics ; Mitochondria/metabolism ; Parkinson Disease/genetics ; Parkinson Disease/metabolism ; Signal Transduction
Language	English
Publishing date	2018-03-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-017-0079-3
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Article ; Online: Acyl-CoA-binding protein (ACBP): a phylogenetically conserved appetite stimulator.

Charmpilas, Nikolaos / Ruckenstuhl, Christoph / Sica, Valentina / Büttner, Sabrina / Habernig, Lukas / Dichtinger, Silvia / Madeo, Frank / Tavernarakis, Nektarios / Bravo-San Pedro, José M / Kroemer, Guido

Cell death & disease

2020 Volume 11, Issue 1, Page(s) 7

Abstract: Recently, we reported that, in mice, hunger causes the autophagy-dependent release of a protein called "acyl-CoA-binding protein" or "diazepam binding inhibitor" (ACBP/DBI) from cells, resulting in an increase in plasma ACBP concentrations. ... ...

Abstract	Recently, we reported that, in mice, hunger causes the autophagy-dependent release of a protein called "acyl-CoA-binding protein" or "diazepam binding inhibitor" (ACBP/DBI) from cells, resulting in an increase in plasma ACBP concentrations. Administration of extra ACBP is orexigenic and obesogenic, while its neutralization is anorexigenic in mice, suggesting that ACBP is a major stimulator of appetite and lipo-anabolism. Accordingly, obese persons have higher circulating ACBP levels than lean individuals, and anorexia nervosa is associated with subnormal ACBP plasma concentrations. Here, we investigated whether ACBP might play a phylogenetically conserved role in appetite stimulation. We found that extracellular ACBP favors sporulation in Saccharomyces cerevisiae, knowing that sporulation is a strategy for yeast to seek new food sources. Moreover, in the nematode Caenorhabditis elegans, ACBP increased the ingestion of bacteria as well as the frequency pharyngeal pumping. These observations indicate that ACBP has a phylogenetically ancient role as a 'hunger factor' that favors food intake.
MeSH term(s)	Animals ; Appetite ; Autophagy ; Caenorhabditis elegans/metabolism ; Diazepam Binding Inhibitor/metabolism ; Feeding Behavior ; Phylogeny ; Saccharomyces cerevisiae/metabolism ; Spores, Fungal/physiology
Chemical Substances	Diazepam Binding Inhibitor
Language	English
Publishing date	2020-01-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-019-2205-x
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Article ; Online: Changes in Liver Lipidomic Profile in G2019S-

Corral Nieto, Yaiza / Yakhine-Diop, Sokhna M S / Moreno-Cruz, Paula / Manrique García, Laura / Gabrielly Pereira, Amanda / Morales-García, José A / Niso-Santano, Mireia / González-Polo, Rosa A / Uribe-Carretero, Elisabet / Durand, Sylvère / Maiuri, Maria Chiara / Paredes-Barquero, Marta / Alegre-Cortés, Eva / Canales-Cortés, Saray / López de Munain, Adolfo / Pérez-Tur, Jordi / Pérez-Castillo, Ana / Kroemer, Guido / Fuentes, José M /

Bravo-San Pedro, José M

Cells

2023 Volume 12, Issue 5

Abstract: The identification of Parkinson's disease (PD) biomarkers has become a main goal for the diagnosis of this neurodegenerative disorder. PD has not only been intrinsically related to neurological problems, but also to a series of alterations in peripheral ... ...

Abstract	The identification of Parkinson's disease (PD) biomarkers has become a main goal for the diagnosis of this neurodegenerative disorder. PD has not only been intrinsically related to neurological problems, but also to a series of alterations in peripheral metabolism. The purpose of this study was to identify metabolic changes in the liver in mouse models of PD with the scope of finding new peripheral biomarkers for PD diagnosis. To achieve this goal, we used mass spectrometry technology to determine the complete metabolomic profile of liver and striatal tissue samples from WT mice, 6-hydroxydopamine-treated mice (idiopathic model) and mice affected by the G2019S-
MeSH term(s)	Animals ; Mice ; Biomarkers ; Disease Models, Animal ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2/genetics ; Lipidomics ; Liver/metabolism ; Metabolomics ; Parkinson Disease/metabolism
Chemical Substances	Biomarkers ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 (EC 2.7.11.1) ; Lrrk2 protein, mouse (EC 2.7.11.1)
Language	English
Publishing date	2023-03-04
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells12050806
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Article: Mitochondria: Key Organelle in Parkinson's Disease.

Gómez-Sánchez, Rubén / Bravo-San Pedro, José M / Gegg, Matthew E / González-Polo, Rosa A / Fuentes, José M

Parkinson's disease

2016 Volume 2016, Page(s) 6230370

Language	English
Publishing date	2016-08-07
Publishing country	United States
Document type	Journal Article
ZDB-ID	2573854-9
ISSN	2042-0080 ; 2090-8083
ISSN (online)	2042-0080
ISSN	2090-8083
DOI	10.1155/2016/6230370
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Article ; Online: The parkinsonian LRRK2 R1441G mutation shows macroautophagy-mitophagy dysregulation concomitant with endoplasmic reticulum stress.

Yakhine-Diop, Sokhna M S / Rodríguez-Arribas, Mario / Canales-Cortés, Saray / Martínez-Chacón, Guadalupe / Uribe-Carretero, Elisabet / Blanco-Benítez, Mercedes / Duque-González, Gema / Paredes-Barquero, Marta / Alegre-Cortés, Eva / Climent, Vicente / Aiastui, Ana / López de Munain, Adolfo / Bravo-San Pedro, José M / Niso-Santano, Mireia / Fuentes, José M / González-Polo, Rosa A

Cell biology and toxicology

2021 Volume 38, Issue 5, Page(s) 889–911

Abstract: Autophagy is a mechanism responsible for the degradation of cellular components to maintain their homeostasis. However, autophagy is commonly altered and compromised in several diseases, including neurodegenerative disorders. Parkinson's disease (PD) can ...

Abstract	Autophagy is a mechanism responsible for the degradation of cellular components to maintain their homeostasis. However, autophagy is commonly altered and compromised in several diseases, including neurodegenerative disorders. Parkinson's disease (PD) can be considered a multifactorial disease because environmental factors, genetic factors, and aging are involved. Several genes are involved in PD pathology, among which the LRRK2 gene and its mutations, inherited in an autosomal dominant manner, are responsible for most genetic PD cases. The R1441G LRRK2 mutation is, after G2019S, the most important in PD pathogenesis. Our results demonstrate a relationship between the R1441G LRRK2 mutation and a mechanistic dysregulation of autophagy that compromises cell viability. This altered autophagy mechanism is associated with organellar stress including mitochondrial (which induces mitophagy) and endoplasmic reticulum (ER) stress, consistent with the fact that patients with this mutation are more vulnerable to toxins related to PD, such as MPP
MeSH term(s)	Endoplasmic Reticulum Stress/genetics ; Humans ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2/genetics ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2/metabolism ; Macroautophagy ; Mitophagy/genetics ; Mutation/genetics ; Parkinson Disease/genetics ; Parkinson Disease/metabolism ; Parkinson Disease/pathology ; Protein Serine-Threonine Kinases/genetics
Chemical Substances	LRRK2 protein, human (EC 2.7.11.1) ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 (EC 2.7.11.1) ; Protein Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2021-05-31
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	48824-0
ISSN	1573-6822 ; 0742-2091
ISSN (online)	1573-6822
ISSN	0742-2091
DOI	10.1007/s10565-021-09617-w
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Article ; Online: Metabolic alterations in plasma from patients with familial and idiopathic Parkinson's disease.

Yakhine-Diop, Sokhna M S / Morales-García, José A / Niso-Santano, Mireia / González-Polo, Rosa A / Uribe-Carretero, Elisabet / Martinez-Chacon, Guadalupe / Durand, Sylvere / Maiuri, Maria Chiara / Aiastui, Ana / Zulaica, Miren / Ruíz-Martínez, Javier / López de Munain, Adolfo / Pérez-Tur, Jordi / Pérez-Castillo, Ana / Kroemer, Guido / Bravo-San Pedro, José M / Fuentes, José M

Aging

2020 Volume 12, Issue 17, Page(s) 16690–16708

Abstract: The research of new biomarkers for Parkinson's disease is essential for accurate and precocious diagnosis, as well as for the discovery of new potential disease mechanisms and drug targets. The main objective of this work was to identify metabolic ... ...

Abstract	The research of new biomarkers for Parkinson's disease is essential for accurate and precocious diagnosis, as well as for the discovery of new potential disease mechanisms and drug targets. The main objective of this work was to identify metabolic changes that might serve as biomarkers for the diagnosis of this neurodegenerative disorder. For this, we profiled the plasma metabolome from mice with neurotoxin-induced Parkinson's disease as well as from patients with familial or sporadic Parkinson's disease. By using mass spectrometry technology, we analyzed the complete metabolome from healthy volunteers compared to patients with idiopathic or familial (carrying the G2019S or R1441G mutations in the
Language	English
Publishing date	2020-09-09
Publishing country	United States
Document type	Journal Article
ISSN	1945-4589
ISSN (online)	1945-4589
DOI	10.18632/aging.103992
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Article: Acetylome in Human Fibroblasts From Parkinson's Disease Patients.

Yakhine-Diop, Sokhna M S / Rodríguez-Arribas, Mario / Martínez-Chacón, Guadalupe / Uribe-Carretero, Elisabet / Gómez-Sánchez, Rubén / Aiastui, Ana / López de Munain, Adolfo / Bravo-San Pedro, José M / Niso-Santano, Mireia / González-Polo, Rosa A / Fuentes, José M

Frontiers in cellular neuroscience

2018 Volume 12, Page(s) 97

Abstract: Parkinson's disease (PD) is a multifactorial neurodegenerative disorder. The pathogenesis of this disease is associated with gene and environmental factors. Mutations in leucine-rich repeat kinase 2 (LRRK2) are the most frequent genetic cause of familial ...

Abstract	Parkinson's disease (PD) is a multifactorial neurodegenerative disorder. The pathogenesis of this disease is associated with gene and environmental factors. Mutations in leucine-rich repeat kinase 2 (LRRK2) are the most frequent genetic cause of familial and sporadic PD. Moreover, posttranslational modifications, including protein acetylation, are involved in the molecular mechanism of PD. Acetylation of lysine proteins is a dynamic process that is modulated in PD. In this descriptive study, we characterized the acetylated proteins and peptides in primary fibroblasts from idiopathic PD (IPD) and genetic PD harboring G2019S or R1441G
Language	English
Publishing date	2018-04-17
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2452963-1
ISSN	1662-5102
ISSN	1662-5102
DOI	10.3389/fncel.2018.00097
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Article ; Online: IFDOTMETER: A New Software Application for Automated Immunofluorescence Analysis.

Rodríguez-Arribas, Mario / Pizarro-Estrella, Elisa / Gómez-Sánchez, Rubén / Yakhine-Diop, S M S / Gragera-Hidalgo, Antonio / Cristo, Alejandro / Bravo-San Pedro, Jose M / González-Polo, Rosa A / Fuentes, José M

Journal of laboratory automation

2016 Volume 21, Issue 2, Page(s) 246–259

Abstract: Most laboratories interested in autophagy use different imaging software for managing and analyzing heterogeneous parameters in immunofluorescence experiments (e.g., LC3-puncta quantification and determination of the number and size of lysosomes). One ... ...

Abstract	Most laboratories interested in autophagy use different imaging software for managing and analyzing heterogeneous parameters in immunofluorescence experiments (e.g., LC3-puncta quantification and determination of the number and size of lysosomes). One solution would be software that works on a user's laptop or workstation that can access all image settings and provide quick and easy-to-use analysis of data. Thus, we have designed and implemented an application called IFDOTMETER, which can run on all major operating systems because it has been programmed using JAVA (Sun Microsystems). Briefly, IFDOTMETER software has been created to quantify a variety of biological hallmarks, including mitochondrial morphology and nuclear condensation. The program interface is intuitive and user-friendly, making it useful for users not familiar with computer handling. By setting previously defined parameters, the software can automatically analyze a large number of images without the supervision of the researcher. Once analysis is complete, the results are stored in a spreadsheet. Using software for high-throughput cell image analysis offers researchers the possibility of performing comprehensive and precise analysis of a high number of images in an automated manner, making this routine task easier.
MeSH term(s)	Fluorescent Antibody Technique/methods ; High-Throughput Screening Assays ; Image Processing, Computer-Assisted/methods ; Software
Language	English
Publishing date	2016-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2211-0690
ISSN (online)	2211-0690
DOI	10.1177/2211068215600650
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Article ; Online: Possible involvement of the relationship of LRRK2 and autophagy in Parkinson's disease.

Bravo-San Pedro, José M / Gómez-Sánchez, Rubén / Niso-Santano, Mireia / Pizarro-Estrella, Elisa / González-Polo, Rosa A / Fuentes, José M

Biochemical Society transactions

2012 Volume 40, Issue 5, Page(s) 1129–1133

Abstract: PD (Parkinson's disease) is a neurodegenerative disorder caused by loss of dopamine-generating cells in the substantia nigra. The implication of genetic factors in the aetiology of PD has an essential importance in our understanding of the development of ...

Abstract	PD (Parkinson's disease) is a neurodegenerative disorder caused by loss of dopamine-generating cells in the substantia nigra. The implication of genetic factors in the aetiology of PD has an essential importance in our understanding of the development of the disease. Mutations in the LRRK2 (leucine-rich repeat kinase 2) gene cause late-onset PD with a clinical appearance indistinguishable from idiopathic PD. Moreover, LRRK2 has been associated with the process of autophagy regulation. Autophagy is an intracellular catabolic mechanism whereby a cell recycles or degrades damaged proteins and cytoplasmic organelles. In the present paper, we discuss the role of LRRK2 in autophagy, and the importance of this relationship in the development of nigral degeneration in PD.
MeSH term(s)	Autophagy ; Humans ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 ; Mutation ; Parkinson Disease/enzymology ; Parkinson Disease/metabolism ; Protein-Serine-Threonine Kinases/chemistry ; Protein-Serine-Threonine Kinases/genetics ; Protein-Serine-Threonine Kinases/metabolism
Chemical Substances	LRRK2 protein, human (EC 2.7.11.1) ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 (EC 2.7.11.1) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2012-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	184237-7
ISSN	1470-8752 ; 0300-5127
ISSN (online)	1470-8752
ISSN	0300-5127
DOI	10.1042/BST20120095
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