Responses of astrocyte to simultaneous glutamate and arachidonic acid treatment

Xu, Zhen; Liu, Hua Dong; Lau, Lok Ting; Zhang, Yingge; Zhao, Rui; Tong, Geng Lei; Chan, Pak H.; Yu, Albert Cheung Hoi

doi:10.1016/j.neuint.2009.02.016

Cited by 10 publications

(9 citation statements)

References 49 publications

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“…Astrocytes, on the other hand, comprise the major cell type population within white and grey matters and perform an array of specialized functions providing anatomical networks and physiological support to regional neurons (Zou et al , 2010). Astrocytes are responsible for the metabolic processing of the amino acids and carbohydrates that are necessary to maintain the balance of antioxidants (Almeida et al , 2002; Lee et al , 2010a), the generation of energy supply (Kreft et al , 2012), the intercellular exchange of metabolic precursors (Hertz, 2011; Maciejewski and Rothman, 2008; Pardo et al , 2011), and regulate neuroinflammatory responses (Lee et al , 2013; Xu et al , 2009). …”

Section: Introductionmentioning

confidence: 99%

Glutamate metabolism and HIV-associated neurocognitive disorders

et al. 2014

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HIV-1 infection can lead to neurocognitive impairment collectively known as HIV-Associated Neurocognitive Disorders (HAND). Although combined antiretroviral treatment (cART) has significantly ameliorated HIV’s morbidity and mortality, persistent neuroinflammation and neurocognitive dysfunction continue. This review focuses on the current clinical and molecular evidence of the viral and host factors that influence glutamate-mediated neurotoxicity and neuropathogenesis as an important underlying mechanism during the course of HAND development. In addition, discusses potential pharmacological strategies targeting the glutamatergic system that may help prevent and improve neurological outcomes in HIV-1 infected subjects.

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Section: Introductionmentioning

confidence: 99%

Glutamate metabolism and HIV-associated neurocognitive disorders

et al. 2014

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“…2Cc, d, arrowheads) on the plasma membrane. We have previously reported that arachidonic acid could induce changes on astrocyte membrane as observed under AFM (Xu et al,2009). Others have reported that peaks resulted from the anchoring cytoskeleton and that tubers were from stiff membrane proteins protruding from the membrane surface (Viitala and Jarnefelt,1985; Nowakowski et al,2001).…”

Section: Discussionmentioning

confidence: 93%

“…Primary cultures of cerebral cortical astrocytes were prepared from newborn ICR mice as described previously (Yu and Hertz,1982; Yu and Lau,2000; Lau and Yu,2001; Dong et al,2009; Xu et al,2009). Primary cultures of microglia were obtained as described by Liva and de Vellis (2001), with minor modification.…”

Section: Methodsmentioning

confidence: 99%

“…Astrocytes, after 12 hr of Glu or NH 4 Cl treatment, were fixed for 30 min in 2.5% glutaraldehyde in 0.9% NaCl, washed three times with distilled water, cut into 1 × 1 cm 2 squares, and immobilized onto a steel disk with double‐sided adhesive tape. AFM image was captured in contact mode with a SPM‐9500J3 scanning probe microscope (Shimadzu Corporation, Tokyo, Japan) as described previously (Xu et al,2009).…”

Section: Methodsmentioning

confidence: 99%

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A new specialization in astrocytes: Glutamate‐ and ammonia‐induced nuclear size changes

Yang¹,

Li²,

Zhou³

et al. 2011

J of Neuroscience Research

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We observed nuclear swelling in glutamate (Glu)-treated astrocytes that was concomitant with but independent of astrocytic cell swelling. We confirmed Glu-induced nuclear swelling with nuclei isolated from astrocytes. Ammonia is metabolically related to Glu and could induce a nuclear swelling in intact astrocytes but shrinkage in isolated nuclei. Other compounds such as glutamine, aspartate, taurine, glycine, and ATP did not cause any nuclear swelling in isolated nuclei of astrocytes. Surprisingly, Glu and ammonia did not induce nuclear swelling in microglia, C6, HEK 293, or Hep G2 cell lines in cultures and their isolated nuclei. The Glu- and ammonia-induced nuclear size changes appear to be a specific response of astrocytes to these two closely related metabolic compounds.

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“…The MDA content of astrocytes was measured as an index of the amount of lipid peroxidation in the cell membrane and carried out according to Xu et al () and Yu et al (). ATP levels were determined with an ATP assay kit (Beyotime, Beijing, China) via the luciferin/luciferase method.…”

Section: Methodsmentioning

confidence: 99%

Ischemia preconditioning protects astrocytes from ischemic injury through 14‐3‐3γ

Pang

Chai

Gao

et al. 2015

J of Neuroscience Research

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Stroke is a leading cause of death and disability, and new strategies are required to reduce neuronal injury and improve prognosis. Ischemia preconditioning (IPC) is an intrinsic phenomenon that protects cells from subsequent ischemic injury and might provide promising mechanisms for clinical treatment. In this study, primary astrocytes exhibited significantly less cell death than control when exposed to different durations of IPC (15, 30, 60, or 120 min). A 15-min duration was the most effective IPC to protect astrocytes from 8-hr-ischemia injury. The protective mechanisms of IPC involve the upregulation of protective proteins, including 14-3-3γ, and attenuation of malondialdehyde (MDA) content and ATP depletion. 14-3-3γ is an antiapoptotic intracellular protein that was significantly upregulated for up to 84 hr after IPC. In addition, IPC promoted activation of the c-Jun N-terminal kinase (JNK), extracellular signal-related kinase (ERK)-1/2, p38, and protein kinase B (Akt) signaling pathways. When JNK was specifically inhibited with SP600125, the upregulation of 14-3-3γ induced by IPC was almost completely abolished; however, there was no effect on ATP or MDA levels. This suggests that, even though both energy preservation and 14-3-3γ up-regulation were turned on by IPC, they were controlled by different pathways. The ERK1/2, p38, and Akt signaling pathways were not involved in the 14-3-3γ upregulation and energy preservation. These results indicate that IPC could protect astrocytes from ischemia injury by inducing 14-3-3γ and by alleviating energy depletion through different pathways, suggesting multiple protection of IPC and providing new insights into potential stroke therapies.

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Responses of astrocyte to simultaneous glutamate and arachidonic acid treatment

Cited by 10 publications

References 49 publications

Glutamate metabolism and HIV-associated neurocognitive disorders

Glutamate metabolism and HIV-associated neurocognitive disorders

A new specialization in astrocytes: Glutamate‐ and ammonia‐induced nuclear size changes

Ischemia preconditioning protects astrocytes from ischemic injury through 14‐3‐3γ

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