Induction of brain aquaporin 9 (AQP9) in catecholaminergic neurons in diabetic rats

Badaut, Jérôme; Brunet, Jean-François; Petit, Jean‐Marie; Guérin, Céline F.; Magistretti, Pierre J.; Regli, Luca

doi:10.1016/j.brainres.2007.10.087

Cited by 29 publications

(25 citation statements)

References 40 publications

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“…It was similar with that after a metabolic stress, AQP9 expression was induced in pyramidal neurons, which did not express this channel in physiological conditions 10 . Up to date, findings of many experiments under many pathological situations in brain about AQP9-positive neurons suggested AQP9 plays an active role in energy balance as a glycerol-lactate-channel in neuron 8,15,16 . Our outcomes also suggested AQP9 might be involved in the energy metabolism of neurons after TBI.…”

Section: Discussionmentioning

confidence: 99%

Aquaporin 9 in rat brain after severe traumatic brain injury

Liu

Yang

Qiu

et al. 2012

Arq. Neuro-Psiquiatr.

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Predominantly caused by motor vehicle accidents, the traumatic brain injury (TBI) is the leading cause of death and severe disability among people under the age of 45 in Western industrialized countries 1 . Almost all patients suffer from severe disorder of energy metabolism 2 , ionic dysfunction 3 , and water homeostasis 4 after TBI. Experimental evidences indicate that aquaporin 9 (AQP9), which is one member of the water channel family in brain, can facilitate the flow of water and permeate glycerol, monocarboxylates, and urea through the plasma membrane and it is involved in water homeostasis and neuronal energy metabolism in brain 5 . In brain ischemia models, the studies show that AQP9 may be a helper in the regulation of postischemic edema 6 . Yet, as far as we know, little is known about AQP9 in brain after TBI. The present study was performed to study whether brain AQP9 expression is altered and what are the possible roles of AQP9 in brain after TBI. ABSTRACT Objective: To reveal the expression and possible roles of aquaporin 9 (AQP9) in rat brain, after severe traumatic brain injury (TBI). Methods: Brain water content (BWC), tetrazolium chloride staining, Evans blue staining, immunohistochemistry (IHC), immunofluorescence (IF), western blot, and real-time polymerase chain reaction were used. Results: The BWC reached the first and second (highest) peaks at 6 and 72 hours, and the blood brain barrier (BBB) was severely destroyed at six hours after the TBI. The worst brain ischemia occurred at 72 hours after TBI. Widespread AQP9-positive astrocytes and neurons in the hypothalamus were detected by means of IHC and IF after TBI. The abundance of AQP9 and its mRNA increased after TBI and reached two peaks at 6 and 72 hours, respectively, after TBI. Conclusions: Increased AQP9 might contribute to clearance of excess water and lactate in the early stage of TBI. Widespread AQP9-positive astrocytes might help lactate move into neurons and result in cellular brain edema in the later stage of TBI. AQP9-positive neurons suggest that AQP9 plays a role in energy balance after TBI. METHODS Experimental animalKey words: aquaporin-9, traumatic brain injury, brain edema. RESuMOObjetivo: Revelar a expressão e os possíveis papéis da aquaporina 9 (AQP9) no cérebro de ratos após lesão cerebral traumática (LCT) grave. Métodos: Foram utilizados: determinação do conteúdo cerebral de água, corante cloreto de tetrazólio, corante azul de Evans, imunoistoquímica (IHQ), imunofluorescência (IF), western blot e PCR em tempo real. Resultados: O conteúdo cerebral de água alcançou o primeiro e o segundo (o mais alto) picos após 6 e 72 horas. A função da barreira hematoencefálica se mostrou muito prejudicada após 6 horas da LCT. A pior isquemia cerebral ocorreu após 72 horas da LCT. Astrócitos AQP9 positivos e neurônios no hipotálamo foram detectados difusamente pela IHQ e IF após LCT. A abundância de AQP9 e de sua mRNA aumentou após LCT e alcançou dois picos após 6 e 72 horas, respectivamente, da LCT. Conclusões: AQP9 aumentada pode contr...

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Section: Discussionmentioning

confidence: 99%

Aquaporin 9 in rat brain after severe traumatic brain injury

Liu

Yang

Qiu

et al. 2012

Arq. Neuro-Psiquiatr.

View full text Add to dashboard Cite

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Section: Aqps In Normal Brain Tissuesmentioning

confidence: 99%

“…AQP9 may play a key role in cellular energy balance as a glycerol channel in the liver and in the brain [24]. AQP9 is increased in catecholaminergic nuclei in diabetic rats [24], further suggesting that it likely participates in neuronal energy balance. In astrocytes, AQP9 can facilitate the diffusion of glycerol and monocarboxylates, which may serve as energy substrates in the central nervous system [21].…”

Section: Aqps In Normal Brain Tissuesmentioning

confidence: 99%

Aquaporins in Cerebrovascular Disease: A Target for Treatment of Brain Edema

2011

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In cerebrovascular disease, edema formation is frequently observed within the first 7 days and is characterized by molecular and cellular changes in the neurovascular unit. The presence of water channels, aquaporins (AQPs), within the neurovascular unit has led to intensive research in understanding the underlying roles of each of the AQPs under normal conditions and in different diseases. In this review, we summarize some of the recent knowledge on AQPs, focusing on AQP4, the most abundant AQP in the central nervous system. Several experimental models illustrate that AQPs have dual, complex regulatory roles in edema formation and resolution. To date, no specific therapeutic agents have been developed to inhibit water flux through these channels. However, experimental results strongly suggest that this is an important area for future investigation. In fact, early inhibition of water channels may have positive effects in the prevention of edema formation. At later time points during the course of disease, AQP is important for the clearance of water from the brain into blood vessels. Thus, AQPs, and in particular AQP4, have important roles in the resolution of edema after brain injury. The function of these water channel proteins makes them an excellent therapeutic target.

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“…Using a model of diabetes mellitus in rats, AQP9 over-expression was reported selectively in neurons of catecholaminergic nuclei, and decreased in brain stem slices after insulin exposure (282). Further, using siRNA in astrocytic cultures, the same group demonstrated reduced glycerol uptake and changes in astrocytic energy metabolism (277).…”

Section: Metabolism and Diabetes Mellitusmentioning

confidence: 98%