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

Yang, Chunzhang; Li, Hui Li; Zhou, Ye; Chai, Rui; Zhao, Rui; Dong, Yan; Xu, Zhen; Lau, Lok Ting; Zhang, Yingge; Jiang, Teng; Chen, Jianguo; Yu, Albert Cheung Hoi

doi:10.1002/jnr.22657

Cited by 7 publications

(7 citation statements)

References 58 publications

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“…Our data indicate that, at least in the context of Gln-deprived Sp2/0 cells, ammonium ions impede nuclear fragmentation and condensation without interfering with caspase activation. The modulation of nuclear size by ammonium ions has been described in astrocytes [ 46 ], and ammonium ions have been shown to increase the activity of phospholipase A2 [ 47 ], an enzyme which was linked to nuclear shrinkage occurring during caspase-independent cell death [ 48 ]. Whether phospholipase A2 plays such a role in Gln-deprived Sp2/0 cells remains to be determined.…”

Section: Discussionmentioning

confidence: 99%

Ammonium ions improve the survival of glutamine-starved hybridoma cells

Abusneina

Gauthier

2016

Cell Biosci

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BackgroundAs a consequence of a reprogrammed metabolism, cancer cells are dependent on the amino acid l-glutamine for their survival, a phenomenon that currently forms the basis for the generation of new, cancer-specific therapies. In this paper, we report on the role which ammonium ions, a product of glutaminolysis, play on the survival of l-glutamine-deprived Sp2/0-Ag14 mouse hybridoma cells.ResultsThe supplementation of l-glutamine-starved Sp2/0-Ag14 cell cultures with either ammonium acetate or ammonium chloride resulted in a significant increase in viability. This effect did not depend on the ability of cells to synthesize l-glutamine, and was not affected by the co-supplementation with α-ketoglutarate. When we examined the effect of ammonium acetate and ammonium chloride on the induction of apoptosis by glutamine deprivation, we found that ammonium salts did not prevent caspase-3 activation or cytochrome c leakage, indicating that they did not act by modulating core apoptotic processes. However, both ammonium acetate and ammonium chloride caused a significant reduction in the number of l-glutamine-starved cells exhibiting apoptotic nuclear fragmentation and/or condensation.ConclusionAll together, our results show that ammonium ions promote the survival of l-glutamine-deprived Sp2/0-Ag14 cells and modulate late-apoptotic events. These findings highlight the complexity of the modulation of cell survival by l-glutamine, and suggest that targeting survival-signaling pathways modulated by ammonium ions should be examined as a potential anti-cancer strategy.

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Section: Discussionmentioning

confidence: 99%

Ammonium ions improve the survival of glutamine-starved hybridoma cells

Abusneina

Gauthier

2016

Cell Biosci

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“…Astrocytes exhibit the most prominent swelling during brain edema (Albertini and Bianchi, 2010;Badaut et al, 2002;Tait et al, 2008;Yang et al, 2011). AQPs in astrocytes therefore play a critical role in water homeostasis in the brain.…”

Section: Discussionmentioning

confidence: 99%

“…Primary cultures of cerebral cortical astrocytes were prepared, as previously described (Dong et al, 2009;Yang et al, 2011;Yu et al, 2001;Zhou et al, 2010), from newborn (within 24 h after birth) ICR mice. Briefly, meninges-free cerebral cortices were cut into small cubes and suspended in modified Dulbecco's Modified Eagle's Medium (DMEM).…”

Section: Primary Cultures Of Cerebral Cortical Astrocytes and Neuronsmentioning

confidence: 99%

AQP5 is differentially regulated in astrocytes during metabolic and traumatic injuries

Chai

Jiang

Wong

et al. 2013

Glia

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Water movement plays vital roles in both physiological and pathological conditions in the brain. Astrocytes are responsible for regulating this water movement and are the major contributors to brain edema in pathological conditions. Aquaporins (AQPs) in astrocytes play critical roles in the regulation of water movement in the brain. AQP1, 3, 4, 5, 8, and 9 have been reported in the brain. Compared with AQP1, 4, and 9, AQP3, 5, and 8 are less studied. Among the lesser known AQPs, AQP5, which has multiple functions identified outside the central nervous system, is also indicated to be involved in hypoxia injury in astrocytes. In our study, AQP5 expression could be detected both in primary cultures of astrocytes and neurons, and AQP5 expression in astrocytes was confirmed in 1- to 4-week old primary cultures of astrocytes. AQP5 was localized on the cytoplasmic membrane and in the cytoplasm of astrocytes. AQP5 expression was downregulated during ischemia treatment and upregulated after scratch-wound injury, which was also confirmed in a middle cerebral artery occlusion model and a stab-wound injury model in vivo. The AQP5 increased after scratch injury was polarized to the migrating processes and cytoplasmic membrane of astrocytes in the leading edge of the scratch-wound, and AQP5 over-expression facilitated astrocyte process elongation after scratch injury. Taken together, these results indicate that AQP5 might be an important water channel in astrocytes that is differentially expressed during various brain injuries.

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“…VitB6 is known to increase gamma-aminobutyric acid (GABA) levels, a major neurotransmitter acting in the inhibition of neurons, and may protect hippocampal CA1 pyramidal cells from ischemic damage [ 36 ]. Additionally, glutamate is an important precursor of GABA and glutamate decarboxylase (GAD) is the main enzyme specialized to synthesize GABA, which uses vitB6 as the cofactor [ 37 ]. Therefore, our data suggests a possible increase in the GAD activity and GABA concentrations although not experimentally validated.…”

Section: Discussionmentioning

confidence: 99%

DNA repair protein APE1 is involved in host response during pneumococcal meningitis and its expression can be modulated by vitamin B6

Coutinho

Oliveira

Witwer

et al. 2017

J Neuroinflammation

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BackgroundThe production of reactive oxygen species (ROS) during pneumococcal meningitis (PM) leads to severe DNA damage in the neurons and is the major cause of cell death during infection. Hence, the use of antioxidants as adjuvant therapy has been investigated. Previous studies have demonstrated the possible participation of apurinic/apyrimidinic endonuclease (APE1) during PM. The aims of this study were to investigate the APE1 expression in the cortical and hippocampal tissues of infant Wistar rats infected with Streptococcus pneumoniae and its association with cell death and understand the role of vitamin B6 (vitB6) as a protective factor against cell death.MethodsAPE1 expression and oxidative stress markers were analyzed at two-time points, 20 and 24 h post infection (p.i.), in the cortex (CX) and hippocampus (HC) of rats supplemented with vitB6. Statistical analyses were performed by the nonparametric Kruskal–Wallis test using Dunn’s post test.ResultsOur results showed high protein levels of APE1 in CX and HC of infected rats. In the CX, at 20 h p.i., vitB6 supplementation led to the reduction of expression of APE1 and apoptosis-inducing factor, while no significant changes in the transcript levels of caspase-3 were observed. Furthermore, levels of carbonyl content and glutamate in the CX were reduced by vitB6 supplementation at the same time point of 20 h p.i.. Since our data showed a significant effect of vitB6 on the CX at 20 h p.i. rather than that at 24 h p.i., we evaluated the effect of administering a second dose of vitB6 at 18 h p.i. and sacrifice at 24 h p.i.. Reduction in the oxidative stress and APE1 levels were observed, although the latter was not significant. Although the levels of APE1 was not significantly changed in the HC with vitB6 adjuvant therapy, vitB6 supplementation prevented the formation of the truncated form of APE1 (34 kDa) that is associated with apoptosis.ConclusionsOur data suggest that PM affects APE1 expression, which can be modulated by vitB6. Additionally, vitB6 contributes to the reduction of glutamate and ROS levels. Besides the potential to reduce cell death and oxidative stress during neuroinflammation, vitB6 showed enhanced effect on the CX than on the HC during PM.

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

Cited by 7 publications

References 58 publications

Ammonium ions improve the survival of glutamine-starved hybridoma cells

Ammonium ions improve the survival of glutamine-starved hybridoma cells

AQP5 is differentially regulated in astrocytes during metabolic and traumatic injuries

DNA repair protein APE1 is involved in host response during pneumococcal meningitis and its expression can be modulated by vitamin B6

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