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AMPKα1 Deficiency in Astrocytes from a Rat Model of ALS Is Associated with an Altered Metabolic Resilience
by
Hermans, Emmanuel
, Belo do Nascimento, Inês
, Ates, Gamze
, Massie, Ann
, Beckers, Pauline
, Desmet, Nathalie
in
Adenosine Triphosphate
/ Adenylic acid
/ AMP-activated protein kinase
/ AMP-Activated Protein Kinases
/ AMPK
/ Amyotrophic lateral sclerosis
/ Amyotrophic Lateral Sclerosis - genetics
/ Animal models
/ Animals
/ Astrocytes
/ ATP
/ Cellular stress response
/ Energy
/ Energy metabolism
/ Enzymes
/ Experiments
/ Gene expression
/ Glucose
/ glutamate transport
/ Glutamic Acid
/ Health aspects
/ Kinases
/ Laboratories
/ metabolic stress
/ Metabolism
/ Motor Neurons
/ mRNA
/ Nervous system
/ Neurons
/ Physiological aspects
/ Protein kinases
/ Protein turnover
/ Proteins
/ Rats
/ Spinal cord
/ Superoxide Dismutase-1 - genetics
2023
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AMPKα1 Deficiency in Astrocytes from a Rat Model of ALS Is Associated with an Altered Metabolic Resilience
by
Hermans, Emmanuel
, Belo do Nascimento, Inês
, Ates, Gamze
, Massie, Ann
, Beckers, Pauline
, Desmet, Nathalie
in
Adenosine Triphosphate
/ Adenylic acid
/ AMP-activated protein kinase
/ AMP-Activated Protein Kinases
/ AMPK
/ Amyotrophic lateral sclerosis
/ Amyotrophic Lateral Sclerosis - genetics
/ Animal models
/ Animals
/ Astrocytes
/ ATP
/ Cellular stress response
/ Energy
/ Energy metabolism
/ Enzymes
/ Experiments
/ Gene expression
/ Glucose
/ glutamate transport
/ Glutamic Acid
/ Health aspects
/ Kinases
/ Laboratories
/ metabolic stress
/ Metabolism
/ Motor Neurons
/ mRNA
/ Nervous system
/ Neurons
/ Physiological aspects
/ Protein kinases
/ Protein turnover
/ Proteins
/ Rats
/ Spinal cord
/ Superoxide Dismutase-1 - genetics
2023
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AMPKα1 Deficiency in Astrocytes from a Rat Model of ALS Is Associated with an Altered Metabolic Resilience
by
Hermans, Emmanuel
, Belo do Nascimento, Inês
, Ates, Gamze
, Massie, Ann
, Beckers, Pauline
, Desmet, Nathalie
in
Adenosine Triphosphate
/ Adenylic acid
/ AMP-activated protein kinase
/ AMP-Activated Protein Kinases
/ AMPK
/ Amyotrophic lateral sclerosis
/ Amyotrophic Lateral Sclerosis - genetics
/ Animal models
/ Animals
/ Astrocytes
/ ATP
/ Cellular stress response
/ Energy
/ Energy metabolism
/ Enzymes
/ Experiments
/ Gene expression
/ Glucose
/ glutamate transport
/ Glutamic Acid
/ Health aspects
/ Kinases
/ Laboratories
/ metabolic stress
/ Metabolism
/ Motor Neurons
/ mRNA
/ Nervous system
/ Neurons
/ Physiological aspects
/ Protein kinases
/ Protein turnover
/ Proteins
/ Rats
/ Spinal cord
/ Superoxide Dismutase-1 - genetics
2023
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AMPKα1 Deficiency in Astrocytes from a Rat Model of ALS Is Associated with an Altered Metabolic Resilience
Journal Article
AMPKα1 Deficiency in Astrocytes from a Rat Model of ALS Is Associated with an Altered Metabolic Resilience
2023
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Overview
Alterations in the activity of the regulator of cell metabolism AMP-activated protein kinase (AMPK) have been reported in motor neurons from patients and animal models of amyotrophic lateral sclerosis (ALS). Considering the key role played by astrocytes in modulating energy metabolism in the nervous system and their compromised support towards neurons in ALS, we examined whether a putative alteration in AMPK expression/activity impacted astrocytic functions such as their metabolic plasticity and glutamate handling capacity. We found a reduced expression of AMPK mRNA in primary cultures of astrocytes derived from transgenic rats carrying an ALS-associated mutated superoxide dismutase (hSOD1G93A). The activation of AMPK after glucose deprivation was reduced in hSOD1G93A astrocytes compared to non-transgenic. This was accompanied by a lower increase in ATP levels and increased vulnerability to this insult, although the ATP production rate did not differ between the two cell types. Furthermore, soliciting the activity of glutamate transporters was found to induce similar AMPK activity in these cells. However, manipulation of AMPK activity did not influence glutamate transport. Together, these results suggest that the altered AMPK responsiveness in ALS might be context dependent and may compromise the metabolic adaptation of astrocytes in response to specific cellular stress.
Publisher
MDPI AG,MDPI
Subject
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