Temporal and Regional Evolution of Aquaporin-4 Expression and Magnetic Resonance Imaging in a Rat Pup Model of Neonatal Stroke

Badaut, Jérôme; Ashwal, Stephen; Tone, Beatriz; Regli, Luca; Tian, Hou Rou; Obenaus, André

doi:10.1203/pdr.0b013e3180db291b

Cited by 82 publications

(79 citation statements)

References 20 publications

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“…In young rats, AQP4 expression was increased 24 h after stroke at the edge of the lesion where there was no significant modification of water content measured by magnetic resonance imaging (Badaut et al, 2007a), suggesting that increased AQP4 expression could limit or prevent the formation and extension of edema. The role of AQP4 in cerebral edema is dual and depends of the model used (Badaut et al, 2007b;Verkman et al, 2006).…”

Section: Discussionmentioning

confidence: 94%

Protective Role of Early Aquaporin 4 Induction against Postischemic Edema Formation

Hirt

Ternon

Price

et al. 2008

J Cereb Blood Flow Metab

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Aquaporin 4 (AQP4) is a water channel involved in water movements across the cell membrane and is spatially organized on the cell surface in orthogonal array particles (OAPs). Its role in edema formation or resolution after stroke onset has been studied mainly at late time points. We have shown recently that its expression is rapidly induced after ischemia coinciding in time with an early swelling of the ischemic hemisphere. There are two isoforms of AQP4: AQP4-M1 and AQP4-M23. The ratio of these isoforms influences the size of the OAPs but the functional impact is not known. The role of the early induction of AQP4 is not yet known. Thrombin preconditioning in mice provides a useful model to study endogenous protective mechanisms. Using this model, we provide evidence for the first time that the early induction of AQP4 may contribute to limit the formation of edema and that the AQP4-M1 isoform is predominantly induced in the ischemic tissue at this time point. Although it prevents edema formation, the early induction of the AQP4 expression does not prevent the blood-brain barrier disruption, suggesting an effect limited to the prevention of edema formation possibly by removing of water from the tissue.

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Section: Discussionmentioning

confidence: 94%

Protective Role of Early Aquaporin 4 Induction against Postischemic Edema Formation

Hirt

Ternon

Price

et al. 2008

J Cereb Blood Flow Metab

Self Cite

125

116

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show abstract

“…AQP4 expression has also been observed at 48 h in transient occlusions. In a mild stroke model (30 min of MCA occlusion), up-regulated AQP4 expression was detected for up to 7 d, whereas in a severe stroke model, elevated AQP4 expression persisted for up to 28 d [32,33] . The pattern of AQP4 expression in cerebrovascular diseases has revealed that this molecule plays a critical role in regulating water movement during brain edema [17] .…”

Section: Discussionmentioning

confidence: 99%

Curcumin attenuates brain edema in mice with intracerebral hemorrhage through inhibition of AQP4 and AQP9 expression

et al. 2015

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Aim: Aquaporins (AQPs) are the water-channels that play important roles in brain water homeostasis and in cerebral edema induced by brain injury. In this study we investigated the relationship between AQPs and a neuroprotective agent curcumin that was effective in the treatment of brain edema in mice with intracerebral hemorrhage (ICH). Methods: ICH was induced in mice by autologous blood infusion. The mice immediately received curcumin (75, 150, and 300 mg/kg, ip). The Rotarod test scores, brain water content and brain expression of AQPs were measured post ICH. Cultured primary mouse astrocytes were used for in vitro experiments. The expression of AQP1, AQP4 and AQP9 and NF-κB p65 were detected using Western blotting or immunochemistry staining. Results: Curcumin administration dose-dependently reduced the cerebral edema at d 3 post ICH, and significantly attenuated the neurological deficits at d 5 post ICH. Furthermore, curcumin dose-dependently decreased the gene and protein expression of AQP4 and AQP9, but not AQP1 post ICH. Treatment of the cultured astrocytes with Fe 2+ (10-100 µmol/L) dose-dependently increased the expression and nuclear translocation of NF-κB p65 and the expression of AQP4 and AQP9, which were partly blocked by co-treatment with curcumin (20 µmol/L) or the NF-κB inhibitor PDTC (10 µmol/L). Conclusion: Curcumin effectively attenuates brain edema in mice with ICH through inhibition of the NF-κB pathway and subsequently the expression of AQP4 and AQP9. Curcumin may serve as a potential therapeutic agent for ICH.

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“…NF200, MBP, and CNPase coronal sections that were immunostained with infrared secondary antibodies were scanned using the same parameters for sham and CCI with a Licor-Odyssey scanner at 21 lm/pixel resolution (Licor BioScience, Lincoln, NE). The infrared method proposed to quantify the immunohistochemistry has recently been described by different authors (Bloch et al, 2011;Wong, 2004), and by our group (Badaut et al, 2007(Badaut et al, ,2011. For surface area measurements of the CC with NF200 (see Fig.…”

Section: Tissue Processing and Immunohistochemistrymentioning

confidence: 99%

Traumatic Brain Injury in Young Rats Leads to Progressive Behavioral Deficits Coincident with Altered Tissue Properties in Adulthood

Ajao

Pop

Adami

et al. 2012

Journal of Neurotrauma

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Traumatic brain injury (TBI) affects many infants and children, and results in enduring motor and cognitive impairments with accompanying changes in white matter tracts, yet few experimental studies in rodent juvenile models of TBI (jTBI) have examined the timeline and nature of these deficits, histologically and functionally. We used a single controlled cortical impact (CCI) injury to the parietal cortex of rats at post-natal day (P) 17 to evaluate behavioral alterations, injury volume, and morphological and molecular changes in gray and white matter, with accompanying measures of electrophysiological function. At 60 days post-injury (dpi), we found that jTBI animals displayed behavioral deficits in foot-fault and rotarod tests, along with a left turn bias throughout their early developmental stages and into adulthood. In addition, anxiety-like behaviors on the zero maze emerged in jTBI animals at 60 dpi. The final lesion constituted only *3% of brain volume, and morphological tissue changes were evaluated using MRI, as well as immunohistochemistry for neuronal nuclei (NeuN), myelin basic protein (MBP), neurofilament-200 (NF200), and oligodendrocytes (CNPase). White matter morphological changes were associated with a global increase in MBP immunostaining and reduced compound action potential amplitudes at 60 dpi. These results suggest that brain injury early in life can induce long-term white matter dysfunction, occurring in parallel with the delayed development and persistence of behavioral deficits, thus modeling clinical and longitudinal TBI observations.

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Temporal and Regional Evolution of Aquaporin-4 Expression and Magnetic Resonance Imaging in a Rat Pup Model of Neonatal Stroke

Cited by 82 publications

References 20 publications

Protective Role of Early Aquaporin 4 Induction against Postischemic Edema Formation

Protective Role of Early Aquaporin 4 Induction against Postischemic Edema Formation

Curcumin attenuates brain edema in mice with intracerebral hemorrhage through inhibition of AQP4 and AQP9 expression

Traumatic Brain Injury in Young Rats Leads to Progressive Behavioral Deficits Coincident with Altered Tissue Properties in Adulthood

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