Astrocytes Express N-Methyl-D-Aspartate Receptor Subunits in Development, Ischemia and Post-Ischemia

Zhou, Ye; Li, Hui Li; Zhao, Rui; Yang, Liang; Dong, Yan; Yue, Xin; Ying, Yao; Wang, Zhuo; Chen, Jianguo; Cui, Cai Lian; Yu, Albert Cheung-Hoi

doi:10.1007/s11064-010-0325-x

Cited by 32 publications

(23 citation statements)

References 66 publications

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“…Extraordinarily, they observed that SNP induced GluN2B localization in the cell nucleus, supporting previous findings suggesting putative NMDAR nuclear translocation [115,116]. On the other hand, Zhou et al [117] characterized NMDAR subunit expression in mouse cultured astrocytes at different times and in a model of ischemia. They found GluN1, GluN2A, and GluN2B expression by RT-PCR and immunofluorescence (only GluN1 and GluN2B).…”

Section: +supporting

confidence: 72%

NMDA Receptors in Astroglia: Chronology, Controversies, and Contradictions from a Complex Molecule

Balderas¹,

GonzálezHernández²

2018

Astrocyte - Physiology and Pathology

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The neurocentric theory dismissed for decades the role of glia in information handling within the central nervous system (CNS). Nevertheless, almost 3 decades ago, this started to change and today astrocytes are considered relevant players for this function. Astrocytes "listen" to neuronal communication, regulate it, and respond at the cellular and synctitial level. Ionotropic glutamate NMDA receptor (NMDAR) is critical in CNS. It mediates synaptic neuronal communication and it is involved in different mechanisms. However, NMDAR is also expressed by astrocytes, but its functional role in these cells has not been deeply investigated and has been a matter of debate in the last decades. In this chapter, we briefly outline NMDAR intracellular transduction pathways initiated by Ca 2+ flux. Then, we review chronologically NMDAR expression and function in astrocytes that have been a source of controversies and apparent contradictions. Finally, some insights are presented regarding NMDAR in astrocytes in the context of the tripartite synapse concept and the recently described Ca 2+ fluxindependent metabotropic-like NMDAR function in astrocytes. Given the complex molecular nature of NMDAR, its critical role, and the relevance of astrocytes, the study of astrocytic NMDAR promises to provide further understanding of CNS physiology and pathology.

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Section: +supporting

confidence: 72%

NMDA Receptors in Astroglia: Chronology, Controversies, and Contradictions from a Complex Molecule

Balderas¹,

GonzálezHernández²

2018

Astrocyte - Physiology and Pathology

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“…Overactivity of NMDARs results in excitotoxicity that may activate microglia (Chang et al, 2008). In addition to presence of NMDARs in neuronal population, a report suggests the presence of NMDARs in development, ischemia and post-ischemic events (Zhou et al, 2010). The studies on animal subjects clearly indicate the involvement of astrocytic glutamate receptor in glial cell signaling (Schipke et al, 2001; Wong, 2006).…”

Section: Discussionmentioning

confidence: 99%

Curcumin-loaded embryonic stem cell exosomes restored neurovascular unit following ischemia-reperfusion injury

Kalani

Chaturvedi

Kamat

et al. 2016

The International Journal of Biochemistry & Cell Biology

200

141

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We tested whether the combined nano-formulation, prepared with curcumin (anti-inflammatory and neuroprotective molecule) and embryonic stem cell exosomes (MESC-exocur), restored neurovascular loss following an ischemia reperfusion (IR) injury in mice. IR-injury was created in 8–10 weeks old mice and divided into two groups. Out of two IR-injured groups, one group received intranasal administration of MESC-exocur for 7 days. Similarly, two sham groups were made and one group received MESC-exocur treatment. The study determined MESC-exocur reduced neurological score, infarct volume and edema following IR-injury. As compared to untreated IR group, MESC-exocur treated-IR group showed reduced inflammation and N-methyl-D-aspartate receptor expression. Treatment of MESC-exocur also reduced astrocytic GFAP expression and alleviated the expression of NeuN positive neurons in IR-injured mice. In addition, MESC-exocur treatment restored vascular endothelial tight (claudin-5 and occludin) and adherent (VE-cadherin) junction proteins in IR-injured mice as compared to untreated IR-injured mice. These results suggest that combining the potentials of embryonic stem cell exosomes and curcumin can help neurovascular restoration following ischemia-reperfusion injury in mice.

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“…For primary cells, ABCA7-deficient mice (ABCA7Ϫ/Ϫ) were cross-bred with TgCRND8 (ABCA7ϩ/ϩ) mice. Primary cultures were prepared from brain of either embryonic 16-day-old (cortical neurons) or postnatal 1-dayold (astrocytes and microglia) mice according to the method of Cole and de Vellis (22), and mixed glial cells were cultured as described previously (23,24). After 20 -24 days of culturing, microglia were harvested by mild trypsinization (25).…”

Section: Methodsmentioning

confidence: 99%

ATP-binding Cassette Transporter A7 (ABCA7) Loss of Function Alters Alzheimer Amyloid Processing

Satoh

Abe-Dohmae

Yokoyama

et al. 2015

Journal of Biological Chemistry

106

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Background:The ATP-binding cassette transporter A7 (ABCA7) is a risk factor for sporadic Alzheimer disease (AD). Results: Loss of ABCA7 promoted A␤ processing and pathology in cell culture and AD mouse models. Conclusion: Altered ABCA7 function may contribute to AD by impacting A␤ production in addition to clearance. Significance: AD-related risk factors may contribute to disease progression through multiple pathways.The ATP-binding cassette transporter A7 (ABCA7) has been identified as a susceptibility factor of late onset Alzheimer disease in genome-wide association studies. ABCA7 has been shown to mediate phagocytosis and affect membrane trafficking. The current study examined the impact of ABCA7 loss of function on amyloid precursor protein (APP) processing and generation of amyloid-␤ (A␤). Suppression of endogenous ABCA7 in several different cell lines resulted in increased ␤-secretase cleavage and elevated A␤. ABCA7 knock-out mice displayed an increased production of endogenous murine amyloid A␤42 species. Crossing ABCA7-deficient animals to an APP transgenic model resulted in significant increases in the soluble A␤ as compared with mice expressing normal levels of ABCA7. Only modest changes in the amount of insoluble A␤ and amyloid plaque densities were observed once the amyloid pathology was well developed, whereas A␤ deposition was enhanced in younger animals. In vitro studies indicated a more rapid endocytosis of APP in ABCA7 knock-out cells that is mechanistically consistent with the increased A␤ production. These in vitro and in vivo findings indicate a direct role of ABCA7 in amyloid processing that may be associated with its primary biological function to regulate endocytic pathways. Several potential loss-of-function ABCA7 mutations and deletions linked to Alzheimer disease that in some instances have a greater impact than apoE allelic variants have recently been identified. A reduction in ABCA7 expression or loss of function would be predicted to increase amyloid production and that may be a contributing factor in the associated Alzheimer disease susceptibility.Genome-wide association studies have identified the ATPbinding cassette transporter A7 (ABCA7) 2 as a susceptibility locus for late onset Alzheimer disease (LOAD) (1, 2). The single nucleotide polymorphisms (SNPs) associated with LOAD are distributed in various domains of the ABCA7 gene and include intronic SNPs and a coding sequence causing G1527A substitution. Studies have identified loci in different clusters, suggesting multiple sites within the ABCA7 gene associated with increased risk for AD (3). However, there is no indication that individuals with at-risk alleles display any differences in ABCA7 expression.ABCA7 is a member of the ATP-binding cassette transporter family largely involved in lipid transport and homeostasis (4). Its highly homologous member ABCA1 has also been linked to LOAD through cholesterol and processing of the amyloid precursor protein (5-7). Overexpression of ABCA7 resulted in a significant decrease in amyloid-...

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Astrocytes Express N-Methyl-D-Aspartate Receptor Subunits in Development, Ischemia and Post-Ischemia

Cited by 32 publications

References 66 publications

NMDA Receptors in Astroglia: Chronology, Controversies, and Contradictions from a Complex Molecule

NMDA Receptors in Astroglia: Chronology, Controversies, and Contradictions from a Complex Molecule

Curcumin-loaded embryonic stem cell exosomes restored neurovascular unit following ischemia-reperfusion injury

ATP-binding Cassette Transporter A7 (ABCA7) Loss of Function Alters Alzheimer Amyloid Processing

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