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Book: The neurochemistry of neuronal death

Massieu, Lourdes

2007

Author's details	ed. Lourdes Massieu
Language	English
Size	234 S. : Ill.
Publisher	Research Signpost
Publishing place	Trivandrum
Publishing country	India
Document type	Book
HBZ-ID	HT015414591
ISBN	81-308-0086-1 ; 978-81-308-0086-8
Database	Catalogue ZB MED Medicine, Health

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Article: The proteomic effects of ketone bodies: implications for proteostasis and brain proteinopathies.

García-Velázquez, Lizbeth / Massieu, Lourdes

Frontiers in molecular neuroscience

2023 Volume 16, Page(s) 1214092

Abstract: A growing body of evidence supports the beneficial effects of the ketone bodies (KBs), acetoacetate and β-hydroxybutyrate (BHB), on diverse physiological processes and diseases. Hence, KBs have been suggested as therapeutic tools for neurodegenerative ... ...

Abstract	A growing body of evidence supports the beneficial effects of the ketone bodies (KBs), acetoacetate and β-hydroxybutyrate (BHB), on diverse physiological processes and diseases. Hence, KBs have been suggested as therapeutic tools for neurodegenerative diseases. KBs are an alternative fuel during fasting and starvation as they can be converted to Ac-CoA to produce ATP. A ketogenic diet (KD), enriched in fats and low in carbohydrates, induces KB production in the liver and favors their use in the brain. BHB is the most abundant KB in the circulation; in addition to its role as energy fuel, it exerts many actions that impact the set of proteins in the cell and tissue. BHB can covalently bind to proteins in lysine residues as a new post-translational modification (PTM) named β-hydroxybutyrylation (Kbhb). Kbhb has been identified in many proteins where Kbhb sites can be critical for binding to other proteins or cofactors. Kbhb is mostly found in proteins involved in chromatin structure, DNA repair, regulation of spliceosome, transcription, and oxidative phosphorylation. Histones are the most studied family of proteins with this PTM, and H3K9bhb is the best studied histone mark. Their target genes are mainly related to cell metabolism, chromatin remodeling and the control of circadian rhythms. The role of Kbhb on physiological processes is poorly known, but it might link KB metabolism to cell signaling and genome regulation. BHB also impacts the proteome by influencing proteostasis. This KB can modulate the Unfolded Protein Response (UPR) and autophagy, two processes involved in the maintenance of protein homeostasis through the clearance of accumulated unfolded and damaged proteins. BHB can support proteostasis and regulate the UPR to promote metabolism adaptation in the liver and prevent cell damage in the brain. Also, BHB stimulates autophagy aiding to the degradation of accumulated proteins. Protein aggregation is common to proteinopathies like Alzheimer's (AD) and Parkinson's (PD) diseases, where the KD and BHB treatment have shown favorable effects. In the present review, the current literature supporting the effects of KBs on proteome conformation and proteostasis is discussed, as well as its possible impact on AD and PD.
Language	English
Publishing date	2023-07-27
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2452967-9
ISSN	1662-5099
ISSN	1662-5099
DOI	10.3389/fnmol.2023.1214092
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Article ; Online: Autophagy as a Homeostatic Mechanism in Response to Stress Conditions in the Central Nervous System.

Gerónimo-Olvera, Cristian / Massieu, Lourdes

Molecular neurobiology

2019 Volume 56, Issue 9, Page(s) 6594–6608

Abstract: Autophagy is considered a major bulk degradation system that helps cells to counteract different intracellular and extracellular stress signals. Several protein complexes integrate multiple signals in order to activate autophagy, which sequesters damaged ...

Abstract	Autophagy is considered a major bulk degradation system that helps cells to counteract different intracellular and extracellular stress signals. Several protein complexes integrate multiple signals in order to activate autophagy, which sequesters damaged cellular components and carries them to lysosomes for degradation. This active mechanism is essential to maintain cell homeostasis and particularly in neurons to sustain their viability. Because of their polarized morphology, neurons face special challenges to recycle cellular components through autophagy in dendrites and distal regions of axons. Thus, autophagy is critical in the remodeling of pre- and post-synaptic constituents to sustain neuronal functionality. Under stress conditions, autophagy may play either a cytotoxic or a cytoprotective role. This discrepancy is partly due to the lack of a full characterization of the autophagic process and conclusive evidence to support whether basal autophagy is stimulated or impaired in a particular condition. Moreover, in many studies, only pharmacologic tools have been used to modulate autophagy. Throughout the present review, we go over the literature revealing autophagy induction in the nervous system under diverse stressful conditions, the signaling pathways involved, and its consequences for neuronal homeostasis and survival. We have focused on five particular stress conditions that alter neuronal homeostasis and can induce neuronal death including, starvation, oxidative stress, endoplasmic reticulum (ER) stress, proteotoxic stress, and aging.
MeSH term(s)	Aging/pathology ; Animals ; Autophagy ; Central Nervous System/pathology ; Homeostasis ; Humans ; Oxidative Stress ; Stress, Physiological
Language	English
Publishing date	2019-03-23
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	645020-9
ISSN	1559-1182 ; 0893-7648
ISSN (online)	1559-1182
ISSN	0893-7648
DOI	10.1007/s12035-019-1546-x
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Article ; Online: Therapeutic strategies for ketosis induction and their potential efficacy for the treatment of acute brain injury and neurodegenerative diseases.

Camberos-Luna, Lucy / Massieu, Lourdes

Neurochemistry international

2019 Volume 133, Page(s) 104614

Abstract: The therapeutic use of ketone bodies (KB) against acute brain injury and neurodegenerative disorders has lately been suggested by many studies. Several mechanisms responsible for the protective action of KB have been described, including metabolic, anti- ... ...

Abstract	The therapeutic use of ketone bodies (KB) against acute brain injury and neurodegenerative disorders has lately been suggested by many studies. Several mechanisms responsible for the protective action of KB have been described, including metabolic, anti-inflammatory and epigenetic. However, it is still not clear whether a specific mechanism of action can be associated with a particular neurological disorder. Different strategies to induce ketosis including the ketogenic diet (KD), caloric restriction (CR), intermittent fasting (IF), as well as the administration of medium chain triglycerides (MCTs), exogenous ketones or KB derivatives, have been used in animal models of brain injury and in humans. They have shown different degrees of success to prevent neuronal damage, motor alterations and cognitive decline. However, more investigation is needed in order to establish safe protocols for clinical application. Throughout the present review, we describe the different approaches that have been used to elevate blood KB and discuss their effectiveness considering their advantages and limitations, as tested in models of brain injury, neurodegeneration and clinical research. We also describe the mechanisms of action of KB in non-pathologic conditions and in association with their protective effect against neuronal damage in acute neurological disorders and neurodegenerative diseases.
MeSH term(s)	Animals ; Brain/metabolism ; Brain Injuries/drug therapy ; Brain Injuries/metabolism ; Caloric Restriction/methods ; Humans ; Ketones/metabolism ; Neurodegenerative Diseases/drug therapy ; Neurodegenerative Diseases/metabolism ; Neurons/metabolism
Chemical Substances	Ketones
Language	English
Publishing date	2019-11-27
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	283190-9
ISSN	1872-9754 ; 0197-0186
ISSN (online)	1872-9754
ISSN	0197-0186
DOI	10.1016/j.neuint.2019.104614
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Article ; Online: Ricardo Tapia (1940 - 2021).

Tovar-Y-Romo, Luis B / Massieu, Lourdes / Arias, Clorinda

Journal of neurochemistry

2021 Volume 159, Issue 6, Page(s) 1045–1046

MeSH term(s)	History, 20th Century ; History, 21st Century ; Humans ; Laboratory Personnel/history ; Male ; Mexico ; Neurosciences/history
Language	English
Publishing date	2021-10-28
Publishing country	England
Document type	Biography ; Historical Article ; Journal Article ; Portrait
ZDB-ID	80158-6
ISSN	1471-4159 ; 0022-3042 ; 1474-1644
ISSN (online)	1471-4159
ISSN	0022-3042 ; 1474-1644
DOI	10.1111/jnc.15526
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Article ; Online: Rescue of Mitochondrial Function in Hutchinson-Gilford Progeria Syndrome by the Pharmacological Modulation of Exportin CRM1.

Monterrubio-Ledezma, Feliciano / Navarro-García, Fernando / Massieu, Lourdes / Mondragón-Flores, Ricardo / Soto-Ponce, Luz Adriana / Magaña, Jonathan J / Cisneros, Bulmaro

Cells

2023 Volume 12, Issue 2

Abstract: Hutchinson-Gilford progeria syndrome (HGPS) is a rare premature aging disorder caused by the expression of progerin, a mutant variant of Lamin A. Recently, HGPS studies have gained relevance because unraveling its underlying mechanism would help to ... ...

Abstract	Hutchinson-Gilford progeria syndrome (HGPS) is a rare premature aging disorder caused by the expression of progerin, a mutant variant of Lamin A. Recently, HGPS studies have gained relevance because unraveling its underlying mechanism would help to understand physiological aging. We previously reported that the CRM1-mediated nuclear protein export pathway is exacerbated in HGPS cells, provoking the mislocalization of numerous protein targets of CRM1. We showed that normalization of this mechanism by pharmacologically inhibiting CRM1 with LMB (specific CRM1 inhibitor), mitigates the senescent phenotype of HGPS cells. Since mitochondrial dysfunction is a hallmark of HGPS, in this study we analyze the effect of LMB on mitochondrial function. Remarkably, LMB treatment induced the recovery of mitochondrial function in HGPS cells, as shown by the improvement in mitochondrial morphology, mitochondrial membrane potential, and ATP levels, which consequently impeded the accumulation of ROS but not mitochondrial superoxide. We provide evidence that the beneficial effect of LMB is mechanistically based on a combinatory effect on mitochondrial biogenesis via upregulation of PGC-1α expression (master transcription cofactor of mitochondrial genes), and mitophagy through the recovery of lysosomal content. The use of exportin CRM1 inhibitors constitutes a promising strategy to treat HGPS and other diseases characterized by mitochondrial impairment.
MeSH term(s)	Humans ; Progeria/drug therapy ; Progeria/genetics ; Progeria/metabolism ; Karyopherins/metabolism ; Aging, Premature/genetics ; Cell Nucleus/metabolism ; Mitochondria/metabolism
Chemical Substances	Karyopherins
Language	English
Publishing date	2023-01-10
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/cells12020275
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Article: Effect of β-Hydroxybutyrate on Autophagy Dynamics During Severe Hypoglycemia and the Hypoglycemic Coma.

Torres-Esquivel, Carmen / Montiel, Teresa / Flores-Méndez, Marco / Massieu, Lourdes

Frontiers in cellular neuroscience

2020 Volume 14, Page(s) 547215

Abstract: Glucose supply from blood is mandatory for brain functioning and its interruption during acute hypoglycemia or cerebral ischemia leads to brain injury. Alternative substrates to glucose such as the ketone bodies (KB), acetoacetate (AcAc), and β- ... ...

Abstract	Glucose supply from blood is mandatory for brain functioning and its interruption during acute hypoglycemia or cerebral ischemia leads to brain injury. Alternative substrates to glucose such as the ketone bodies (KB), acetoacetate (AcAc), and β-hydroxybutyrate (BHB), can be used as energy fuels in the brain during hypoglycemia and prevent neuronal death, but the mechanisms involved are still not well understood. During glucose deprivation adaptive cell responses can be activated such as autophagy, a lysosomal-dependent degradation process, to support cell survival. However, impaired or excessive autophagy can lead to cell dysfunction. We have previously shown that impaired autophagy contributes to neuronal death induced by glucose deprivation in cortical neurons and that D isomer of BHB (D-BHB) reestablishes the autophagic flux increasing viability. Here, we aimed to investigate autophagy dynamics in the brain of rats subjected to severe hypoglycemia (SH) without glucose infusion (GI), severe hypoglycemia followed by GI (SH + GI), and a brief period of hypoglycemic coma followed by GI (Coma). The effect of D-BHB administration after the coma was also tested (Coma + BHB). The transformation of LC3-I to LC3-II and the abundance of autophagy proteins, Beclin 1 (BECN1), ATG7, and ATG12-ATG5 conjugate, were analyzed as an index of autophagosome formation, and the levels of sequestrosome1/p62 (SQSTM1/p62) were determined as a hallmark of autophagic degradation. Data suggest that autophagosomes accumulate in the cortex and the hippocampus of rats after SH, likely due to impaired autophagic degradation. In the cortex, autophagosome accumulation persisted at 6 h after GI in animals exposed to SH but recovered basal levels at 24 h, while in the hippocampus no significant effect was observed. In animals subjected to coma, autophagosome accumulation was observed at 24 h after GI in both regions. D-BHB treatment reduced LC3-II and SQSTM1/p62 content and reduced ULK1 phosphorylation by AMPK, suggesting it stimulates the autophagic flux and decreases AMPK activity reducing autophagy initiation. D-BHB also reduced the number of degenerating cells. Together, data suggest different autophagy dynamics after GI in rats subjected to SH or the hypoglycemic coma and support that D-BHB treatment can modulate autophagy dynamics favoring the autophagic flux.
Language	English
Publishing date	2020-09-23
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2452963-1
ISSN	1662-5102
ISSN	1662-5102
DOI	10.3389/fncel.2020.547215
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Article: IRE1α RIDD activity induced under ER stress drives neuronal death by the degradation of 14-3-3 θ mRNA in cortical neurons during glucose deprivation.

Gómora-García, Juan Carlos / Gerónimo-Olvera, Cristian / Pérez-Martínez, Xochitl / Massieu, Lourdes

Cell death discovery

2021 Volume 7, Issue 1, Page(s) 131

Abstract: Altered protein homeostasis is associated with neurodegenerative diseases and acute brain injury induced under energy depletion conditions such as ischemia. The accumulation of damaged or unfolded proteins triggers the unfolded protein response (UPR), ... ...

Abstract	Altered protein homeostasis is associated with neurodegenerative diseases and acute brain injury induced under energy depletion conditions such as ischemia. The accumulation of damaged or unfolded proteins triggers the unfolded protein response (UPR), which can act as a homeostatic response or lead to cell death. However, the factors involved in turning and adaptive response into a cell death mechanism are still not well understood. Several mechanisms leading to brain injury induced by severe hypoglycemia have been described but the contribution of the UPR has been poorly studied. Cell responses triggered during both the hypoglycemia and the glucose reinfusion periods can contribute to neuronal death. Therefore, we have investigated the activation dynamics of the PERK and the IRE1α branches of the UPR and their contribution to neuronal death in a model of glucose deprivation (GD) and glucose reintroduction (GR) in cortical neurons. Results show a rapid activation of the PERK/p-eIF2α/ATF4 pathway leading to protein synthesis inhibition during GD, which contributes to neuronal adaptation, however, sustained blockade of protein synthesis during GR promotes neuronal death. On the other hand, IRE1α activation occurs early during GD due to its interaction with BAK/BAX, while ASK1 is recruited to IRE1α activation complex during GR promoting the nuclear translocation of JNK and the upregulation of Chop. Most importantly, results show that IRE1α RNase activity towards its splicing target Xbp1 mRNA occurs late after GR, precluding a homeostatic role. Instead, IRE1α activity during GR drives neuronal death by positively regulating ASK1/JNK activity through the degradation of 14-3-3 θ mRNA, a negative regulator of ASK and an adaptor protein highly expressed in brain, implicated in neuroprotection. Collectively, results describe a novel regulatory mechanism of cell death in neurons, triggered by the downregulation of 14-3-3 θ mRNA induced by the IRE1α branch of the UPR.
Language	English
Publishing date	2021-06-03
Publishing country	United States
Document type	Journal Article
ISSN	2058-7716
ISSN	2058-7716
DOI	10.1038/s41420-021-00518-9
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Article ; Online: Role of NADPH oxidase-2 in the progression of the inflammatory response secondary to striatum excitotoxic damage.

Hernández-Espinosa, Diego Rolando / Massieu, Lourdes / Montiel, Teresa / Morán, Julio

Journal of neuroinflammation

2019 Volume 16, Issue 1, Page(s) 91

Abstract: Background: During excitotoxic damage, neuronal death results from the increase in intracellular calcium, the induction of oxidative stress, and a subsequent inflammatory response. NADPH oxidases (NOX) are relevant sources of reactive oxygen species ( ... ...

Abstract	Background: During excitotoxic damage, neuronal death results from the increase in intracellular calcium, the induction of oxidative stress, and a subsequent inflammatory response. NADPH oxidases (NOX) are relevant sources of reactive oxygen species (ROS) during excitotoxic damage. NADPH oxidase-2 (NOX-2) has been particularly related to neuronal damage and death, as well as to the resolution of the subsequent inflammatory response. As ROS are crucial components of the regulation of inflammatory response, in this work, we evaluated the role of NOX-2 in the progression of inflammation resulting from glutamate-induced excitotoxic damage of the striatum in an in vivo model. Methods: The striata of wild-type C57BL/6 J and NOX-2 KO mice (gp91 Results: Our results show a neuroprotective effect in mice with a genetic inhibition of NOX-2, which is partially due to a differential response to excitotoxic damage, characterized by the production of anti-inflammatory cytokines. In NOX-2 KO animals, the excitotoxic condition increased the production of interleukin-4, which could contribute to the production of interleukin-10 that decreased neuronal apoptotic death and the magnitude of striatal injury. Treatment with interleukin-4 and interleukin-10 protected from excitotoxic damage in wild-type animals. Conclusions: The release of proinflammatory cytokines during the excitotoxic event promotes an additional apoptotic death of neurons that survived the initial damage. During the subsequent inflammatory response to excitotoxic damage, ROS generated by NOX-2 play a decisive role in the extension of the lesion and consequently in the severity of the functional compromise, probably by regulating the anti-inflammatory cytokines production.
MeSH term(s)	Animals ; Corpus Striatum/enzymology ; Corpus Striatum/immunology ; Corpus Striatum/pathology ; Disease Progression ; Glutamic Acid/toxicity ; Inflammation/enzymology ; Inflammation/immunology ; Inflammation/pathology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; NADPH Oxidase 2/metabolism
Chemical Substances	Glutamic Acid (3KX376GY7L) ; Cybb protein, mouse (EC 1.6.3.-) ; NADPH Oxidase 2 (EC 1.6.3.-)
Language	English
Publishing date	2019-04-17
Publishing country	England
Document type	Journal Article
ISSN	1742-2094
ISSN (online)	1742-2094
DOI	10.1186/s12974-019-1478-4
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Article ; Online: Treatment with the Ketone Body D-β-hydroxybutyrate Attenuates Autophagy Activated by NMDA and Reduces Excitotoxic Neuronal Damage in the Rat Striatum In Vivo.

Montiel, Teresa / Montes-Ortega, Luis A / Flores-Yáñez, Susana / Massieu, Lourdes

Current pharmaceutical design

2020 Volume 26, Issue 12, Page(s) 1377–1387

Abstract: Background: The ketone bodies (KB), β-hydroxybutyrate (BHB) and acetoacetate, have been proposed for the treatment of acute and chronic neurological disorders, however, the molecular mechanisms involved in KB protection are not well understood. KB can ... ...

Abstract	Background: The ketone bodies (KB), β-hydroxybutyrate (BHB) and acetoacetate, have been proposed for the treatment of acute and chronic neurological disorders, however, the molecular mechanisms involved in KB protection are not well understood. KB can substitute for glucose and support mitochondrial metabolism increasing cell survival. We have reported that the D-isomer of BHB (D-BHB) stimulates autophagic degradation during glucose deprivation in cultured neurons increasing cell viability. Autophagy is a lysosomal degradation process of damaged proteins and organelles activated during nutrient deprivation to obtain building blocks and energy. However, impaired or excessive autophagy can contribute to neuronal death. Objective: The aim of the present study was to test whether D-BHB can preserve autophagic function in an in vivo model of excitotoxic damage induced by the administration of the glutamate receptor agonist, N-methyl-Daspartate (NMDA), in the rat striatum. Methods: D-BHB was administered through an intravenous injection followed by either an intraperitoneal injection (i.v+i.p) or a continuous epidural infusion (i.v+pump), or through a continuous infusion of D-BHB alone. Changes in the autophagy proteins ATG7, ATG5, BECLIN 1 (BECN1), LC3, Sequestrosome1/p62 (SQSTM1/ p62) and the lysosomal membrane protein LAMP2, were evaluated by immunoblot. The lesion volume was measured in cresyl violet-stained brain sections. Results: Autophagy is activated early after NMDA injection but autophagic degradation is impaired due to the cleavage of LAMP2. Twenty-four h after NMDA intrastriatal injection, the autophagic flux is re-established, but LAMP2 cleavage is still observed. The administration of D-BHB through the i.v+pump protocol reduced the content of autophagic proteins and the cleavage of LAMP2, suggesting decreased autophagosome formation and lysosomal membrane preservation, improving autophagic degradation. D-BHB also reduced brain injury. The i.v+i.p administration protocol and the infusion of D-BHB alone showed no effect on autophagy activation or degradation.
MeSH term(s)	3-Hydroxybutyric Acid ; Animals ; Autophagy ; Ketone Bodies/chemistry ; N-Methylaspartate ; Neurons/chemistry ; Neurons/physiology ; Rats
Chemical Substances	Ketone Bodies ; N-Methylaspartate (6384-92-5) ; 3-Hydroxybutyric Acid (TZP1275679)
Language	English
Publishing date	2020-01-18
Publishing country	United Arab Emirates
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1304236-1
ISSN	1873-4286 ; 1381-6128
ISSN (online)	1873-4286
ISSN	1381-6128
DOI	10.2174/1381612826666200115103646
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