Increased expression of aquaporin-4 with methylmercury exposure in the brain of the common marmoset

Yamamoto, Megumi; Takeya, Motohiro; Ikeshima-Kataoka, Hiroko; Yasui, Masato; Kawasaki, Yousuke; Shiraishi, Masayuki; Majima, Eiji; Shiraishi, Seiji; Uezono, Yasuhito; Sasaki, Masanori; Eto, Komyo

doi:10.2131/jts.37.749

Cited by 27 publications

(26 citation statements)

References 29 publications

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“…Previous studies have demonstrated that aquaporin-4 (AQP4) is implicated in the formation and resolution of brain edema, which is one important consequence of cerebral ischemia. [31][32][33][34] Zeng et al 35) found that 10% hypertonic saline exerted anti-edema effects possibly through downregulation of AQP4 expression in the perivascular astrocytes. Hua et al 36) also found that AQP4 played an important role in modulating brain water transport in an astrocytic oxygen-glucose deprivation and reintroduction model.…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of Ginsenoside Rg1 on Astrocytes and Cerebral Ischemic-Reperfusion Mice

Sun¹,

Lai²,

Huang³

et al. 2014

Biological & Pharmaceutical Bulletin

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Ginsenoside Rg1 (Rg1), one of the active ingredients in Panax ginseng, has been known to regulate many cellular processes. The purpose of this study was to investigate the protective effects of Rg1 on apoptosis in mouse cultured astrocytes in vitro and a mouse model of cerebral ischemia and reperfusion in vivo. The cell apoptosis was measured by fluorescence microplate reader and xCELLigence system and the Ca 2 overload was recorded by confocal microscopy. The mitochondrial membrane potential and reactive oxygen species (ROS) were determined by flow cytometry. BALB/c mice were subjected to transient middle cerebral artery occlusion (MCAO) and randomly divided into four groups: Sham (sham-operated 0.9% saline), MCAO (MCAO 0.9% saline), Rg1-L (MCAO Rg1 20 mg/kg) and Rg1-H (MCAO Rg1 40 mg/kg). Neurological deficit scores, brain water content and infarct volume were evaluated at 24 h after reperfusion. The results showed that Rg1 significantly attenuated H 2 O 2 -induced apoptosis in astrocytes. Rg1 efficiently inhibited intracellular Ca 2 overload, loss of mitochondrial membrane potential, and ROS production in astrocytes. In vivo study, it was also observed that Rg1 markedly reduced the neurological deficit scores, brain edema, and infarct volume in the model mice. These results suggest that Rg1 possesses significant neuroprotective effects, which might be related to the prevention of astrocytes from apoptosis.

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Section: Discussionmentioning

confidence: 99%

Protective Effects of Ginsenoside Rg1 on Astrocytes and Cerebral Ischemic-Reperfusion Mice

Sun¹,

Lai²,

Huang³

et al. 2014

Biological & Pharmaceutical Bulletin

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“…Microglia‐derived Iba1 levels are also used as a marker of brain injury (Imai and Kohsaka, ). Immunohistochemistry (IHC) on paraffin‐embedded tissue sections in the sagittal planes was performed as previously described (Yamamoto et al ., ). Primary antibodies were GFAP (Z0334, DAKO Japan, Tokyo, Japan), Iba1 (019–19741; Wako Pure Chemical) and CD204 (clone 2F8; Serotec, Oxford, UK).…”

Section: Methodsmentioning

confidence: 97%

Increased methylmercury toxicity related to obesity in diabetic KK‐Ay mice

Yamamoto

Yanagisawa

Motomura

et al. 2013

J of Applied Toxicology

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We examined the toxic effects of methylmercury (MeHg) in KK-Ay type 2 diabetic mice to clarify how metabolic changes associated with type 2 diabetes mellitus affect MeHg toxicity. MeHg (5 mg Hg kg (-1) day(-1) p.o.) was given to 4-week-old male KK-Ay and C57BL/6J (BL/6) mice three times per week for 6 weeks. Average body weights (BW) of vehicle-treated BL/6 and KK-Ay mice were 16.3 and 16.4 g respectively on the first day, and 24.8 and 42.3 g respectively on the last day of the experiment. MeHg-treated KK-Ay mice began to lose weight about 5 weeks after MeHg administration. Six of seven MeHg-treated KK-Ay mice showed hind-limb clasping in the final stage of the experiment. The mean blood mercury level of MeHg-treated KK-Ay mice reached a maximum of 9.8 µg ml(-1) , whereas that of the MeHg-treated BL/6 mice was 2.8 µg ml(-1) after 10 days of treatment. The average total mercury concentrations in the cerebrum and epididymal fat pad were 7.4 and 0.57 µg g(-1) , respectively, for BL/6 mice and 27 and 1.6 µg g(-1) , respectively, for KK-Ay mice. In MeHg-treated KK-Ay mice with neurological symptoms, CD204-positive macrophages were observed in the brain, kidney and spleen, indicating CD204 could be a marker for injured tissues. BW loss and significant pathological changes were not observed in other groups of mice. These results indicate that body fat gain in type 2 diabetes mellitus and low mercury accumulation in adipose tissue increased MeHg concentrations in organs and enhanced toxicity in KK-Ay mice at the same dose of MeHg per BW.

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“…Methylmercury (MeHg)-treated common marmosets showed lesions in the cerebrum, cerebellum, and peripheral nerves as a model of Minamata disease [94,95], and a slight increase in AQP4 was observed in the reactive astrocytes [96]. …”

Section: Aqp4 In Reactive Astrocytesmentioning

confidence: 99%

Neuroimmunological Implications of AQP4 in Astrocytes

Ikeshima-Kataoka

2016

IJMS

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121

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The brain has high-order functions and is composed of several kinds of cells, such as neurons and glial cells. It is becoming clear that many kinds of neurodegenerative diseases are more-or-less influenced by astrocytes, which are a type of glial cell. Aquaporin-4 (AQP4), a membrane-bound protein that regulates water permeability is a member of the aquaporin family of water channel proteins that is expressed in the endfeet of astrocytes in the central nervous system (CNS). Recently, AQP4 has been shown to function, not only as a water channel protein, but also as an adhesion molecule that is involved in cell migration and neuroexcitation, synaptic plasticity, and learning/memory through mechanisms involved in long-term potentiation or long-term depression. The most extensively examined role of AQP4 is its ability to act as a neuroimmunological inducer. Previously, we showed that AQP4 plays an important role in neuroimmunological functions in injured mouse brain in concert with the proinflammatory inducer osteopontin (OPN). The aim of this review is to summarize the functional implication of AQP4, focusing especially on its neuroimmunological roles. This review is a good opportunity to compile recent knowledge and could contribute to the therapeutic treatment of autoimmune diseases through strategies targeting AQP4. Finally, the author would like to hypothesize on AQP4’s role in interaction between reactive astrocytes and reactive microglial cells, which might occur in neurodegenerative diseases. Furthermore, a therapeutic strategy for AQP4-related neurodegenerative diseases is proposed.

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Increased expression of aquaporin-4 with methylmercury exposure in the brain of the common marmoset

Cited by 27 publications

References 29 publications

Protective Effects of Ginsenoside Rg1 on Astrocytes and Cerebral Ischemic-Reperfusion Mice

Protective Effects of Ginsenoside Rg1 on Astrocytes and Cerebral Ischemic-Reperfusion Mice

Increased methylmercury toxicity related to obesity in diabetic KK‐Ay mice

Neuroimmunological Implications of AQP4 in Astrocytes

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