Shotgun proteomics implicates extracellular matrix proteins and protease systems in neuronal development induced by astrocyte cholinergic stimulation

Moore, Nadia H.; Costa, Lucio G.; Shaffer, Scott A.; Guizzetti, Marina

doi:10.1111/j.0022-3042.2008.05836.x

Cited by 12 publications

(13 citation statements)

References 64 publications

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“…The conditioned medium-harvested from the co-culturescontained several agrin fragments. As expected, this medium also contained thousands of other peptides, including several growth factors (Moore et al 2009).…”

Section: Camassa Et Al: Factors Governing Astrocytic Aqp4 Polaritysupporting

confidence: 62%

Mislocalization of AQP4 precedes chronic seizures in the kainate model of temporal lobe epilepsy

et al. 2013

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It has been suggested that loss of the astrocytic water channel aquaporin-4 (AQP4) from perivascular endfeet in sclerotic hippocampi contributes to increased seizure propensity in human mesial temporal lobe epilepsy (MTLE). Whether this loss occurs prior to or as a consequence of epilepsy development remains to be resolved. In the present study, we investigated whether the expression and distribution of AQP4 was altered prior to (i.e., in the latent phase) or after the onset of chronic epileptic seizures (i.e., in the chronic phase) in the kainate (KA) model of MTLE. Immunogold electron microscopic analysis revealed that AQP4 density in adluminal endfoot membranes was reduced in KA treated rats already in the latent phase, while the AQP4 density in the abluminal endfoot membrane was stable or slightly increased. The decrease in adluminal AQP4 immunogold labeling was accompanied by a reduction in the density of AQP4's anchoring protein alpha-syntrophin. The latent and chronic phases were associated with an upregulation of the M1 isoform of AQP4, as judged by semi-quantitative Western blot analysis. Taken together, the findings in this model suggest that a mislocalization of AQP4--reflecting a loss of astrocyte polarization--is an integral part of the epileptogenic process.

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Section: Camassa Et Al: Factors Governing Astrocytic Aqp4 Polaritysupporting

confidence: 62%

Mislocalization of AQP4 precedes chronic seizures in the kainate model of temporal lobe epilepsy

et al. 2013

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“…The conditioned medium—harvested from the co‐cultures—contained several agrin fragments. As expected, this medium also contained thousands of other peptides, including several growth factors (Moore et al ).…”

Section: Discussionmentioning

confidence: 53%

Mechanisms underlying AQP4 accumulation in astrocyte endfeet

Camassa

Lunde

Hoddevik

et al. 2015

Glia

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The brain-blood interface holds the key to our understanding of how cerebral blood flow is regulated and how water and solutes are exchanged between blood and brain. The highly specialized astrocytic membranes that enwrap brain microvessels are salient constituents of the brain-blood interface. These endfoot membranes contain a distinct set of molecules that is anchored to the subendothelial basal lamina forming an endfoot-basal lamina junctional complex. Here we explore the mechanisms underpinning the formation of this complex. By use of a tailor made model system we show that endothelial cells promote AQP4 accumulation by exerting an inductive effect through extracellular matrix components such as agrin, as well as through a direct mechanical interaction with the endfoot processes. Through the compounds they secrete, the endothelial cells also increase AQP4 expression. The present data suggest that the highly specialized gliovascular interface is established through inductive processes that include both chemical and mechanical factors. GLIA 2015;63:2073-2091.

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“…Increasing research focused on astrocytes should discover humoral factors that are responsible for neuron-glia interactions. It has been reported that thousands of proteins are released from astrocytes in the presence of cholinergic agonist, proinflammatory cytokines, angiogenin, -amyloid peptide 1-42 and lipopolysaccharide (LPS) (Delcourt et al, 2005;Keene et al, 2009;Lafon-Cazal et al, 2003;Lai et al, 2013;Moore et al, 2009;Skorupa et al, 2013). In the present study, we focused on alterations in the levels of proteins released from astrocytes after innate immune activation by treatment with polyI:C, as we have reported that polyI:C impairs the dendritic elongation of hippocampal neurons through astrocyte-derived humoral factors (Ibi et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

Matrix metalloproteinase-3 is a possible mediator of neurodevelopmental impairment due to polyI:C-induced innate immune activation of astrocytes

Yamada

Nagai

Nakai

et al. 2014

Brain, Behavior, and Immunity

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Increasing epidemiological evidence indicates that prenatal infection and childhood central nervous system infection with various viral pathogens enhance the risk for several neuropsychiatric disorders. Polyriboinosinic-polyribocytidilic acid (polyI:C) is known to induce strong innate immune responses that mimic immune activation by viral infections. Our previous findings suggested that activation of the innate immune system in astrocytes results in impairments of neurite outgrowth and spine formation, which lead to behavioral abnormalities in adulthood. To identify candidates of astrocyte-derived humoral factors that affect neuronal development, we analyzed astrocyte-conditioned medium (ACM) from murine astrocyte cultures treated with polyI:C (polyI:C-ACM) by two-dimensional fluorescence difference gel electrophoresis (2D-DIGE). Through a quantitative proteomic screen, we found that 13 protein spots were differentially expressed compared with ACM from vehicle-treated astrocytes (control-ACM), and characterized one of the candidates, matrix metalloproteinase-3 (Mmp3). PolyI:C treatment significantly increased the expression levels of Mmp3 mRNA and protein in astrocytes, but not microglia. PolyI:C-ACM was associated with significantly higher Mmp3 protein level and enzyme activity than control-ACM. The addition of recombinant Mmp3 into culture media impaired dendritic elongation of primary cultured hippocampal neurons, while the deleterious effect of polyI:C-ACM on neurite elongation was attenuated by knockdown of Mmp3 in astrocytes. These results suggest that Mmp3 is a possible mediator of polyI:C-ACM-induced neurodevelopmental impairment.

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Shotgun proteomics implicates extracellular matrix proteins and protease systems in neuronal development induced by astrocyte cholinergic stimulation

Cited by 12 publications

References 64 publications

Mislocalization of AQP4 precedes chronic seizures in the kainate model of temporal lobe epilepsy

Mislocalization of AQP4 precedes chronic seizures in the kainate model of temporal lobe epilepsy

Mechanisms underlying AQP4 accumulation in astrocyte endfeet

Matrix metalloproteinase-3 is a possible mediator of neurodevelopmental impairment due to polyI:C-induced innate immune activation of astrocytes

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