Structural organization of the perivascular astrocyte endfeet and their relationship with the endothelial glucose transporter: A confocal microscopy study

Kacem, Kamel; Lacombe, Pierre; Seylaz, Jacques; Bonvento, Gilles

doi:10.1002/(sici)1098-1136(199805)23:1<1::aid-glia1>3.0.co;2-b

Cited by 320 publications

(184 citation statements)

References 23 publications

(32 reference statements)

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“…**P<0.01 (analyzed using one-way ANOVA followed by Newman-Keuls multiple comparison test) for K104Stop-MCP1 compared with FL-MCP1 at each timepoint. and astrocytes (Guillemin and Brew, 2004); the BMECs, which connect to each other through TJPs, forming the primary barrier, whereas astrocytes, which cover more than 99% of the microvessels with their endfeet, confer a secondary barrier (Kacem et al, 1998;Simard et al, 2003). Here, we used two different in vitro BBB models to assess the effect of plasmin on MCP1-induced BBB compromise.…”

Section: Discussionmentioning

confidence: 99%

“…To better replicate the in vivo BBB conditions, we used a mouse BMEC-astrocyte co-culture system, as astrocytes contribute to the impermeability of BBB by covering more than 99% of the microvessels (Kacem et al, 1998;Simard et al, 2003). Consistent with previous data, in the absence of A2AP, FL-and K104Stop-MCP1 reduced TEER values and increased Evans Blue infiltration substantially (data not shown), whereas, in the presence of A2AP, only K104Stop-MCP1 was effective in compromising the integrity of this in vitro BBB model ( Fig.…”

Section: Truncation By Plasmin Promotes Mcp1-induced Bbb Compromisementioning

confidence: 99%

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Truncation of monocyte chemoattractant protein 1 by plasmin promotes blood–brain barrier disruption

Yao

Tsirka

2011

Journal of Cell Science

102

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SummaryPrevious studies have shown that plasmin cleaves monocyte chemoattractant protein 1 (MCP1; officially known as C-C motif chemokine 2, CCL2) at K104, and this cleavage enhances its chemotactic potency significantly. Accumulating evidence reveals that MCP1 also disrupts the integrity of the blood-brain barrier (BBB). Here, we show that K104Stop-MCP1, truncated at the K104 where plasmin would normally cleave, is more efficient than the full-length protein (FL-MCP1) in compromising the integrity of the BBB in in vitro and in vivo models. K104Stop-MCP1 increases the permeability of BBB in both wild-type mice and mice deficient for tissue plasminogen activator (tPA), which converts plasminogen into active plasmin, suggesting that plasmin-mediated truncation of MCP1 plays an important role in BBB compromise. Furthermore, we show that the mechanisms underlying MCP1-induced BBB disruption involve redistribution of tight junction proteins (occludin and ZO-1) and reorganization of the actin cytoskeleton. Finally, we show that the redistribution of ZO-1 is mediated by phosphorylation of ezrin-radixin-moesin (ERM) proteins. These findings identify plasmin as a key signaling molecule in the regulation of BBB integrity and suggest that plasmin inhibitors might be used to modulate diseases accompanied by BBB compromise.

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Section: Discussionmentioning

confidence: 99%

Section: Truncation By Plasmin Promotes Mcp1-induced Bbb Compromisementioning

confidence: 99%

Truncation of monocyte chemoattractant protein 1 by plasmin promotes blood–brain barrier disruption

Yao

Tsirka

2011

Journal of Cell Science

102

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“…Therefore, potential Env One enlightening example centers on the importance of GLUT1 in the metabolic exchanges between intracerebral vessels and nerve terminals via glial cells in general and astrocytes in particular Voutsinos-Porche et al, 2003;Bonvento et al, 2005). Indeed, the privileged anatomical relationship between astrocyte endfeet that project into the vasculature and individual endothelial cells of the blood-brain barrier (Kacem et al, 1998) provide tracks to explore in HTLV-associated neuropathophysiological effects. Ex vivo studies of interactions between these different cell types placed in the presence of HTLV-1 or different types of HTLV-1-infected cells will help a better understanding of HTLV spreading and pathology.…”

Section: Discussionmentioning

confidence: 99%

HTLV-1 tropism and envelope receptor

et al. 2005

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The identification of CD4 as the primary receptor for HIV followed shortly after the discovery of the virus, but the HTLV receptor remained long elusive, until its recent identification as the GLUT1 glucose transporter. In the present review, we describe the status of the literature that surrounded this discovery as well as the in vitro and in vivo observations that led to the identification of GLUT1. Also, we will explore a few tracks to conciliate the in vitro and in vivo data on HTLV-1 tropism within the context of the HTLV literature that has accumulated over the past 25 years. A close examination of these data leads us to conclude that the preferential detection of HTLV-1 in CD4 þ T lymphocyte subsets in vivo, even in the absence of leukemia, is not likely to be directly related to envelope receptor interactions, but rather to an array of postentry selection bottlenecks in vivo. Furthermore, we propose that infection of other hematopoietic and nonhematopoietic cells is likely to take place during the lifetime of an individual, with a burst early during the infection. Oncogene (2005) 24, 6016-6025.

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“…3 They also extend numerous processes that connect via end-feet, blood vessels to the neurons and the extracellular space. 4 Some of these processes ensheath neurons while others are interconnected with other astrocytes via gap junctions to form astrocytic syncitia. 5 The astrocyte-neuron lactate shuttle hypothesis (ANLS), 6 has profoundly altered our understanding of brain metabolism.…”

Section: Introductionmentioning

confidence: 99%

Functional Astrocyte-Neuron Lactate Shuttle in a Human Stem Cell-Derived Neuronal Network

Tarczyluk

Nagel

O’Neil

et al. 2013

J Cereb Blood Flow Metab

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The NT2.D1 cell line is one of the most well-documented embryocarcinoma cell lines, and can be differentiated into neurons and astrocytes. Great focus has also been placed on defining the electrophysiological properties of the neuronal cells, and more recently we have investigated the functional properties of their associated astrocytes. We now show for the first time that human stem cellderived astrocytes produce glycogen and that co-cultures of these cells demonstrate a functional astrocyte-neuron lactate shuttle (ANLS). The ANLS hypothesis proposes that during neuronal activity, glutamate released into the synaptic cleft is taken up by astrocytes and triggers glucose uptake, which is converted into lactate and released via monocarboxylate transporters for neuronal use. Using mixed cultures of NT2-derived neurons and astrocytes, we have shown that these cells modulate their glucose uptake in response to glutamate. Additionally, we demonstrate that in response to increased neuronal activity and under hypoglycaemic conditions, co-cultures modulate glycogen turnover and increase lactate production. Similar results were also shown after treatment with glutamate, potassium, isoproterenol, and dbcAMP. Together, these results demonstrate for the first time a functional ANLS in a human stem cell-derived co-culture.

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Structural organization of the perivascular astrocyte endfeet and their relationship with the endothelial glucose transporter: A confocal microscopy study

Cited by 320 publications

References 23 publications

Truncation of monocyte chemoattractant protein 1 by plasmin promotes blood–brain barrier disruption

Truncation of monocyte chemoattractant protein 1 by plasmin promotes blood–brain barrier disruption

HTLV-1 tropism and envelope receptor

Functional Astrocyte-Neuron Lactate Shuttle in a Human Stem Cell-Derived Neuronal Network

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