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Cell-specific modulation of monocarboxylate transporter expression contributes to the metabolic reprograming taking place following cerebral ischemia

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Název: Cell-specific modulation of monocarboxylate transporter expression contributes to the metabolic reprograming taking place following cerebral ischemia
Autoři: K. Rosafio, X. Castillo, L. Hirt, L. Pellerin
Zdroj: Neuroscience, vol. 317, pp. 108-120
Informace o vydavateli: Elsevier BV, 2016.
Rok vydání: 2016
Témata: Male, Monocarboxylic Acid Transporters, Neurons, 0301 basic medicine, Analysis of Variance, Time Factors, Brain, Infarction, Middle Cerebral Artery, S100 Calcium Binding Protein beta Subunit, Functional Laterality, Up-Regulation, Disease Models, Animal, Mice, 03 medical and health sciences, 0302 clinical medicine, Phosphopyruvate Hydratase, Reperfusion, Animals, Microtubule-Associated Proteins, Brain/metabolism, Brain/pathology, Infarction, Middle Cerebral Artery/metabolism, Infarction, Middle Cerebral Artery/pathology, Infarction, Middle Cerebral Artery/physiopathology, Microtubule-Associated Proteins/metabolism, Monocarboxylic Acid Transporters/metabolism, Neurons/metabolism, Phosphopyruvate Hydratase/metabolism, S100 Calcium Binding Protein beta Subunit/metabolism, Up-Regulation/physiology
Popis: Monocarboxylate transporters (MCTs) are involved in lactate trafficking and utilization by brain cells. As lactate is not only overproduced during ischemia but its utilization was shown to be essential upon recovery, we analyzed the expression of the main cerebral MCTs at 1 and 24h after an ischemic insult induced by a transient occlusion of the left middle cerebral artery (MCAO) in CD1 mice (n=5, 7 and 10 for control, 1 and 24h groups, respectively). After 1h of reperfusion, an upregulation of the three MCTs was observed in the striatum (MCT1 ipsilateral 2.73 ± 0.2 and contralateral 2.01 ± 0.4; MCT2 ipsilateral 2.1 ± 0.1; MCT4 ipsilateral 1.65 ± 0.1) and in the surrounding cortex of both the ipsilateral (MCT1 2.4 ± 0.4; MCT2 1.62 ± 0.2; MCT4 1.31 ± 0.1) and contralateral (MCT1 2.78 ± 0.4; MCT2 1.76 ± 0.2) hemispheres, compared to the corresponding sham hemispheres. An increase of MCT1 (ipsilateral 2.1 ± 0.2) and MCT2 (contralateral 1.9 ± 0.1) expression was also observed in the hippocampus, while no effect was observed for MCT4. At 24h of reperfusion, total MCT2 and MCT4 expressions were decreased in the striatum (MCT2 ipsilateral 0.32 ± 0.1 and contralateral 0.63 ± 0.1; MCT4 ipsilateral 0.59 ± 0.1) and the surrounding cortex (MCT4 ipsilateral 0.67 ± 0.1), compared to the sham. At the cellular level, neurons which usually express only MCT2 strongly expressed MCT1 at both time points. Surprisingly, staining for MCT4 appeared on neurons and was strong at 24h post-insult, in the striatum and the cortex of both hemispheres. A similar expression pattern was observed also in the ipsilateral hemisphere of the sham operated animals at 24h. Overall, our study indicates that cell-specific changes in MCT expression induced by an ischemic insult may participate to the metabolic adaptations taking place in the brain after a transient ischemic episode.
Druh dokumentu: Article
Popis souboru: application/pdf
Jazyk: English
ISSN: 0306-4522
DOI: 10.1016/j.neuroscience.2015.12.052
Přístupová URL adresa: https://serval.unil.ch/resource/serval:BIB_4E8A8109812E.P001/REF.pdf
https://pubmed.ncbi.nlm.nih.gov/26751713
https://serval.unil.ch/notice/serval:BIB_4E8A8109812E
https://www.ncbi.nlm.nih.gov/pubmed/26751713
https://europepmc.org/article/MED/26751713
https://www.sciencedirect.com/science/article/pii/S0306452215011458
https://core.ac.uk/display/77145405
https://serval.unil.ch/resource/serval:BIB_4E8A8109812E.P001/REF.pdf
https://serval.unil.ch/resource/serval:BIB_4E8A8109812E.P001/REF.pdf
http://nbn-resolving.org/urn/resolver.pl?urn=urn:nbn:ch:serval-BIB_4E8A8109812E6
https://serval.unil.ch/notice/serval:BIB_4E8A8109812E
Rights: Elsevier TDM
Přístupové číslo: edsair.doi.dedup.....bb31e718cd85e64f7c1ce3a363ab02ed
Databáze: OpenAIRE
Popis
Abstrakt:Monocarboxylate transporters (MCTs) are involved in lactate trafficking and utilization by brain cells. As lactate is not only overproduced during ischemia but its utilization was shown to be essential upon recovery, we analyzed the expression of the main cerebral MCTs at 1 and 24h after an ischemic insult induced by a transient occlusion of the left middle cerebral artery (MCAO) in CD1 mice (n=5, 7 and 10 for control, 1 and 24h groups, respectively). After 1h of reperfusion, an upregulation of the three MCTs was observed in the striatum (MCT1 ipsilateral 2.73 ± 0.2 and contralateral 2.01 ± 0.4; MCT2 ipsilateral 2.1 ± 0.1; MCT4 ipsilateral 1.65 ± 0.1) and in the surrounding cortex of both the ipsilateral (MCT1 2.4 ± 0.4; MCT2 1.62 ± 0.2; MCT4 1.31 ± 0.1) and contralateral (MCT1 2.78 ± 0.4; MCT2 1.76 ± 0.2) hemispheres, compared to the corresponding sham hemispheres. An increase of MCT1 (ipsilateral 2.1 ± 0.2) and MCT2 (contralateral 1.9 ± 0.1) expression was also observed in the hippocampus, while no effect was observed for MCT4. At 24h of reperfusion, total MCT2 and MCT4 expressions were decreased in the striatum (MCT2 ipsilateral 0.32 ± 0.1 and contralateral 0.63 ± 0.1; MCT4 ipsilateral 0.59 ± 0.1) and the surrounding cortex (MCT4 ipsilateral 0.67 ± 0.1), compared to the sham. At the cellular level, neurons which usually express only MCT2 strongly expressed MCT1 at both time points. Surprisingly, staining for MCT4 appeared on neurons and was strong at 24h post-insult, in the striatum and the cortex of both hemispheres. A similar expression pattern was observed also in the ipsilateral hemisphere of the sham operated animals at 24h. Overall, our study indicates that cell-specific changes in MCT expression induced by an ischemic insult may participate to the metabolic adaptations taking place in the brain after a transient ischemic episode.
ISSN:03064522
DOI:10.1016/j.neuroscience.2015.12.052