Astrocyte-neuron metabolic cooperation shapes brain activity

Bonvento, Gilles; Bolaños, Juan P.

doi:10.1016/j.cmet.2021.07.006

Cited by 235 publications

(189 citation statements)

References 204 publications

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“…This therapeutic goal may be achieved by stimulating glycolytic enzymes downstream of 1,3-BPG or by inhibiting upstream enzymes. At the same time, these interventions need to ensure that overall energy metabolism and the delicate metabolic interplay between different cell types in the brain are maintained ( 60 ). It has recently been found that PGK activators can improve the outcome of experimental Parkinson’s models ( 61 ).…”

Section: Discussionmentioning

confidence: 99%

Parkinson's disease protein PARK7 prevents metabolite and protein damage caused by a glycolytic metabolite

Heremans

Caligiore

Gerin

et al. 2022

Proc. Natl. Acad. Sci. U.S.A.

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Cells are continuously exposed to potentially dangerous compounds. Progressive accumulation of damage is suspected to contribute to neurodegenerative diseases and aging, but the molecular identity of the damage remains largely unknown. Here we report that PARK7, an enzyme mutated in hereditary Parkinson’s disease, prevents damage of proteins and metabolites caused by a metabolite of glycolysis. We found that the glycolytic metabolite 1,3-bisphosphoglycerate (1,3-BPG) spontaneously forms a novel reactive intermediate that avidly reacts with amino groups. PARK7 acts by destroying this intermediate, thereby preventing the formation of proteins and metabolites with glycerate and phosphoglycerate modifications on amino groups. As a consequence, inactivation of PARK7 (or its orthologs) in human cell lines, mouse brain, and Drosophila melanogaster leads to the accumulation of these damaged compounds, most of which have not been described before. Our work demonstrates that PARK7 function represents a highly conserved strategy to prevent damage in cells that metabolize carbohydrates. This represents a fundamental link between metabolism and a type of cellular damage that might contribute to the development of Parkinson’s disease.

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Section: Discussionmentioning

confidence: 99%

Parkinson's disease protein PARK7 prevents metabolite and protein damage caused by a glycolytic metabolite

Heremans

Caligiore

Gerin

et al. 2022

Proc. Natl. Acad. Sci. U.S.A.

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“…The brain offers an extraordinary example of metabolic cooperation between cells. The high energetic demand of neurons is satisfied by an efficient cooperation between astrocytes and neurons [ 94 ]. The former is glycolytic and generates and releases lactate that is taken by neurons to perform oxidative phosphorylation.…”

Section: Scs Under Different Metabolic Conditionsmentioning

confidence: 99%

Regulation and functional role of the electron transport chain supercomplexes

Cogliati

Alarcón

Enrı́quez

2021

Biochemical Society Transactions

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Mitochondria are one of the most exhaustively investigated organelles in the cell and most attention has been paid to the components of the mitochondrial electron transport chain (ETC) in the last 100 years. The ETC collects electrons from NADH or FADH2 and transfers them through a series of electron carriers within multiprotein respiratory complexes (complex I to IV) to oxygen, therefore generating an electrochemical gradient that can be used by the F1-F0-ATP synthase (also named complex V) in the mitochondrial inner membrane to synthesize ATP. The organization and function of the ETC is a continuous source of surprises. One of the latest is the discovery that the respiratory complexes can assemble to form a variety of larger structures called super-complexes (SCs). This opened an unexpected level of complexity in this well-known and fundamental biological process. This review will focus on the current evidence for the formation of different SCs and will explore how they modulate the ETC organization according to the metabolic state. Since the field is rapidly growing, we also comment on the experimental techniques used to describe these SC and hope that this overview may inspire new technologies that will help to advance the field.

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“…Astrocytes participate in the transport of substances between the CNS and the circulatory system, which prevents the invasion of harmful substances such as circulating antigens (Iadecola and Nedergaard, 2007;Nuriya et al, 2013) and regulate the twoway exchange of water as well as solutes on both sides of the BBB (Fukuda and Badaut, 2012;Shi Z. F. et al, 2021). What is more, astrocytes sense changes in neuronal metabolism and activate their calcium channels, releasing transmitters to regulate blood vessel diameter and blood flow to meet neuronal oxygen and energy needs (Gordon et al, 2007(Gordon et al, , 2011Marina et al, 2020;Bonvento and Bolaños, 2021). Nevertheless, after the stroke, BBB damage leads to continuous leakage of blood components, which leads astrocytes to activate and convert dramatically.…”

Section: Roles Of Reactive Astrocytes In Neuro-inflammationmentioning

confidence: 99%

The Specific Role of Reactive Astrocytes in Stroke

Han

et al. 2022

Front. Cell. Neurosci.

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Astrocytes are essential in maintaining normal brain functions such as blood brain barrier (BBB) homeostasis and synapse formation as the most abundant cell type in the central nervous system (CNS). After the stroke, astrocytes are known as reactive astrocytes (RAs) because they are stimulated by various damage-associated molecular patterns (DAMPs) and cytokines, resulting in significant changes in their reactivity, gene expression, and functional characteristics. RAs perform multiple functions after stroke. The inflammatory response of RAs may aggravate neuro-inflammation and release toxic factors to exert neurological damage. However, RAs also reduce excitotoxicity and release neurotrophies to promote neuroprotection. Furthermore, RAs contribute to angiogenesis and axonal remodeling to promote neurological recovery. Therefore, RAs’ biphasic roles and mechanisms make them an effective target for functional recovery after the stroke. In this review, we summarized the dynamic functional changes and internal molecular mechanisms of RAs, as well as their therapeutic potential and strategies, in order to comprehensively understand the role of RAs in the outcome of stroke disease and provide a new direction for the clinical treatment of stroke.

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Astrocyte-neuron metabolic cooperation shapes brain activity

Cited by 235 publications

References 204 publications

Parkinson's disease protein PARK7 prevents metabolite and protein damage caused by a glycolytic metabolite

Parkinson's disease protein PARK7 prevents metabolite and protein damage caused by a glycolytic metabolite

Regulation and functional role of the electron transport chain supercomplexes

The Specific Role of Reactive Astrocytes in Stroke

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