Tau Phosphorylation and Sevoflurane Anesthesia

H, Le Freche; Brouillette, Jonathan; Fernandez-Gomez, Francisco-José; Patin, Pauline; Caillierez, Raphaëlle; Zommer, Nadège; Sergeant, Nicolas; Buée-Scherrer,; Lebuffe, Gilles; Blum, David; Buée, Luc

doi:10.1097/aln.0b013e31824be8c7

Cited by 189 publications

(96 citation statements)

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“…Moreover, while the multiple exposures of sevoflurane from P6 to P8 still induced Tau phosphorylation at P10 (Figure 2C and 2D), the single exposure of sevoflurane anesthesia at P6 did not induce Tau phosphorylation at P6 (Figure 2A and 2B). These findings suggested that the Tau phosphorylation resulted from multiple exposures of sevoflurane but not a single exposure of sevoflurane, which were consistent with the results from the studies by Shen et al 9 and Le Freche et al 45 .…”

Section: Discussionsupporting

confidence: 89%

“…Specifically, repeated exposures (once every month for five months) of sevoflurane in 5 to 6 month-old mice induced Tau phosphorylation and cognitive impairment in the mice 45 . However, the effects of the sevoflurane anesthesia (e.g., 3% sevoflurane two hours daily for three days) on Tau phosphorylation in young mice have not been investigated.…”

Section: Introductionmentioning

confidence: 99%

“…Anesthetic-induced hypothermia 41–43 , and anesthetic isoflurane 44 , sevoflurane 45 , and propofol 46 have been reported to induce Tau phosphorylation in vitro and in hippocampus of adult mice. Specifically, repeated exposures (once every month for five months) of sevoflurane in 5 to 6 month-old mice induced Tau phosphorylation and cognitive impairment in the mice 45 .…”

Section: Introductionmentioning

confidence: 99%

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Sevoflurane Induces Tau Phosphorylation and Glycogen Synthase Kinase 3β Activation in Young Mice

et al. 2014

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Background Children with multiple exposures to anesthesia and surgery may have an increased risk of developing cognitive impairment. Sevoflurane is a commonly used anesthetic in children. Tau phosphorylation contributes to cognitive dysfunction. We therefore assessed the effects of sevoflurane on Tau phosphorylation and underlying mechanisms in young mice. Methods Six day-old wild-type (WT) and Tau knockout (KO) mice were exposed to sevoflurane. We determined the effects of the sevoflurane anesthesia on Tau phosphorylation, levels of the kinases and phosphatase related to Tau phosphorylation, interleukin-6, and postsynaptic density protein 95 (PSD-95) in hippocampus, and cognitive function in both young WT and Tau KO mice. Results Anesthesia with 3% sevoflurane two hours daily for three days induced Tau phosphorylation (257% versus 100%, P=0.0025, n=6), enhanced activation of glycogen synthase kinase 3β (GSK3β), the kinase related to Tau phosphorylation in the hippocampus of postnatal day 8 WT mice. The sevoflurane anesthesia decreased hippocampus PSD-95 levels and induced cognitive impairment in the postnatal day 31 mice. GSK3β inhibitor lithium inhibited the sevoflurane-induced GSK3β activation, Tau phosphorylation, elevated levels of interleukin-6 and cognitive impairment in the WT young mice. Finally, the sevoflurane anesthesia did not induce an elevation of interleukin-6 levels, reduction in PSD-5 levels in hippocampus, or cognitive impairment in Tau KO young mice. Conclusions These data suggested that sevoflurane induced Tau phosphorylation, GSK3β activation, elevation of interleukin-6 and reduction of PSD-95 levels in hippocampus of young mice, and cognitive impairment in the mice. Future studies will dissect the cascade relationship of these effects.

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Section: Discussionsupporting

confidence: 89%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Sevoflurane Induces Tau Phosphorylation and Glycogen Synthase Kinase 3β Activation in Young Mice

et al. 2014

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“…Also the pharmacological drugs effect on proteolysis pathways, given that pI and MW identification of the truncated forms may provide the cleavage site according to the antibody's epitope 34 . Interestingly, recent data have elucidated using mini-2DE the association of lifestyle and drug treatments with cognitive impairments in mouse models, as well as the biochemical profile of a new Tau mutation [35][36][37] .…”

Section: Discussionmentioning

confidence: 99%

Consensus Brain-derived Protein, Extraction Protocol for the Study of Human and Murine Brain Proteome Using Both 2D-DIGE and Mini 2DE Immunoblotting

Fernandez-Gomez

Jumeau

Derisbourg

et al. 2014

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“…боты синапсов, сопровождаясь снижением когнитивных функций [9,10,11]. Токсичность тау-протеина связана с ацетилированием двух лизинов (K274 и K281), кото-рые блокируют долговременные потенциалы в синапсах гиппокампа и приводят к нарушению памяти [12].…”

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Tauopathy and cognitive impairment in experimental diabetes mellitus

et al. 2017

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Обучение и психосоциальные аспекты Education and psychosocial aspectТаупатии и когнитивные нарушения ау-протеин, ассоциированный с микротрубоч-ками центральной нервной системы (ЦНС), представляет собой белок цитоскелета, регули-рующий развитие нейронов и способствующий сборке и стабильности микротрубочек, которые являются важ-ными для транспорта везикул в ЦНС. В человеческом мозге семейство тау-белков представлено шестью изо-формами в диапазоне от 352 до 441 аминокислот, получен-ных из одного гена путем альтернативного сплайсинга [1]. Амино-концевой остаток тау-протеина (или «область проекции» микротрубочек) взаимодействует с плаз-матической мембраной. Карбоксиконцевая область характеризуется наличием 3 или 4 повторов, которые обе-спечивают свойства тау-белков для стабилизации микро-трубочек, способствуют их полимеризации. Эти функции негативно регулируются с помощью фосфорилирования в нескольких местах (и вокруг) связывающего домена ми-кротрубочек. Этот процесс может проходить с участием нескольких киназ [2,3]. Почти 20% от тау-белка фосфо-рилируется в физиологических условиях [4]. Внутрикле-точные агрегаты избыточно гиперфосфорилированного тау-белка характеризуют группу нейродегенеративных заболеваний под названием «таупатии» [5,6,7]. Все та-упатии делятся на спорадические нейродегенеративные заболевания (прогрессирующий надъядерный паралич, мультисистемная атрофия, деменция с тельцами Леви, болезнь Альцгеймера (БА) и др.) и ирритативные (болезнь Гентингтона, Вильсона-Коновалова, Фара и др.) [8].Патогенез таупатий включает накопление тау-белка в головном мозге и прогрессирующее нарушение ра-

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Tau Phosphorylation and Sevoflurane Anesthesia

Abstract: Background: There is a growing interest in the involvement of anesthetic agents in the etiology of postoperative cognitive dysfunction. Recent animal studies suggest that acute anes-

Cited by 189 publications

References 59 publications

Sevoflurane Induces Tau Phosphorylation and Glycogen Synthase Kinase 3β Activation in Young Mice

Sevoflurane Induces Tau Phosphorylation and Glycogen Synthase Kinase 3β Activation in Young Mice

Consensus Brain-derived Protein, Extraction Protocol for the Study of Human and Murine Brain Proteome Using Both 2D-DIGE and Mini 2DE Immunoblotting

Tauopathy and cognitive impairment in experimental diabetes mellitus

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