Osmotic swelling characteristics of glial cells in the murine hippocampus, cerebellum, and retina <i>in situ</i>

Hirrlinger, Petra G.; Wurm, Antje; Hirrlinger, Johannes; Bringmann, Andreas; Reichenbach, Andreas

doi:10.1111/j.1471-4159.2008.05243.x

Cited by 49 publications

(51 citation statements)

References 50 publications

(133 reference statements)

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“…In addition, marked intracellular swelling of the perivascular astroglial foot processes was present in patients who died in ALF-induced coma (Kato et al, 1992). In vitro experiments have also reported astrocyte swelling, by assessing the intracellular space using [ 3 H]-3-O-methylglucose ( Norenberg et al, 1991), or by microscopic measurements of cellular volume ( Hirrlinger et al, 2008), following the addition of pathogenic factors associated with HE. In CLD, astrocytes present a characteristic morphology, known as Alzheimer type II astrocytosis: large, swollen cells with enlarged swollen nuclei and cytoplasm, margination of chromatin, mitochondrial and rough endoplasmic reticulum proliferation and accumulation of glycogen ( Norenberg, 1977).…”

Section: Astrocyte Swelling and Brain Edema In Liver Disease/failurementioning

confidence: 98%

Brain edema in acute liver failure and chronic liver disease: Similarities and differences

Bosoi

Rose

2013

Neurochemistry International

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Hepatic encephalopathy (HE) is a complex neuropsychiatric syndrome that typically develops as a result of acute liver failure or chronic liver disease. Brain edema is a common feature associated with HE. In acute liver failure, brain edema contributes to an increase in intracranial pressure, which can fatally lead to brain stem herniation. In chronic liver disease, intracranial hypertension is rarely observed, even though brain edema may be present. This discrepancy in the development of intracranial hypertension in acute liver failure versus chronic liver disease suggests that brain edema plays a different role in relation to the onset of HE. Furthermore, the pathophysiological mechanisms involved in the development of brain edema in acute liver failure and chronic liver disease are dissimilar. This review explores the types of brain edema, the cells, and pathogenic factors involved in its development, while emphasizing the differences in acute liver failure versus chronic liver disease. The implications of brain edema developing as a neuropathological consequence of HE, or as a cause of HE, are also discussed. HighlightsBrain edema is a common feature in ALF and CLD. HE is inconsistently associated with the presence of brain edema. Fibrous and protoplasmic astrocytes are differentially implicated in the pathogenesis of HE. The pathogenesis of HE is multifactorial causing an array of neurological symptoms.

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Section: Astrocyte Swelling and Brain Edema In Liver Disease/failurementioning

confidence: 98%

Brain edema in acute liver failure and chronic liver disease: Similarities and differences

Bosoi

Rose

2013

Neurochemistry International

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“…Indeed, it has been shown that the decrease in the extracellular space volume in retinal slices superfused with glutamate is lower than expected when only the swelling of neuronal cell bodies is considered [51]. Usually, superfusion of retinal slices with a hypoosmotic solution does not induce a swelling of Müller cells for 10-15 min [25,31,57].…”

Section: Introductionmentioning

confidence: 95%

Mechanisms of VEGF- and Glutamate-Induced Inhibition of Osmotic Swelling of Murine Retinal Glial (Müller) Cells: Indications for the Involvement of Vesicular Glutamate Release and Connexin-Mediated ATP Release

et al. 2011

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We determined the mechanisms of glutamate and ATP release from murine retinal glial (Müller) cells by pharmacological manipulation of the vascular endothelial growth factor (VEGF)- and glutamate-induced inhibition of cellular swelling under hypoosmotic conditions. It has been shown that exogenous glutamate inhibits hypoosmotic swelling of rat Müller cells via the induction of the release of ATP (Uckermann et al. in J Neurosci Res 83:538-550, 53). VEGF was shown to inhibit hypoosmotic swelling of rat Müller cells by inducing the release of glutamate (Wurm et al. in J Neurochem 104:386-399, 55). The swelling-inhibitory effect of VEGF in murine Müller cells was blocked by an inhibitor of vesicular exocytosis, by a modulator of the allosteric site of vesicular glutamate transporters, and by inhibitors of phospholipase C and protein kinase C. The swelling-inhibitory effect of glutamate in murine Müller cells was prevented by inhibitors of connexin hemichannels. The effects of both VEGF and glutamate were blocked by tetrodotoxin and by an inhibitor of T-type voltage-gated calcium channels. Murine Müller cells display connexin-43 immunoreactivity. The data suggest that Müller cells of the murine retina may release glutamate by vesicular exocytosis, whereas ATP is released through connexin hemichannels.

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“…5). It has been shown that murine retinal glial cells maintain their cell volume constant up to 20 min of hypotonic exposure before cellular swelling becomes obvious (56). The lack of significant cellular swelling under these conditions can be explained by the activation of an endogenous purinergic signaling cascade (57).…”

Section: Gpr34-deficient Mice Show No Obvious Phenotype Under Specifimentioning

confidence: 99%

Altered Immune Response in Mice Deficient for the G Protein-coupled Receptor GPR34

Liebscher¹,

Müller

Teupser

et al. 2011

Journal of Biological Chemistry

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103

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The X-chromosomal GPR34 gene encodes an orphan G i protein-coupled receptor that is highly conserved among vertebrates. To evaluate the physiological relevance of GPR34, we generated a GPR34-deficient mouse line. GPR34-deficient mice were vital, reproduced normally, and showed no gross abnormalities in anatomical, histological, laboratory chemistry, or behavioral investigations under standard housing. Because GPR34 is highly expressed in mononuclear cells of the immune system, mice were specifically tested for altered functions of these cell types. Following immunization with methylated BSA, the number of granulocytes and macrophages in spleens was significantly lower in GPR34-deficient mice as in wild-type mice. GPR34-deficient mice showed significantly increased paw swelling in the delayed type hypersensitivity test and higher pathogen burden in extrapulmonary tissues after pulmonary infection with Cryptococcus neoformans compared with wild-type mice. The findings in delayed type hypersensitivity and infection tests were accompanied by significantly different basal and stimulated TNF-␣, GM-CSF, and IFN-␥ levels in GPR34-deficient animals. Our data point toward a functional role of GPR34 in the cellular response to immunological challenges. G protein-coupled receptors (GPCR)2 form the largest gene family among transmembrane receptors, including more than 900 genes in humans and other mammals (1). A great number of stimuli, such as light, hormones, neurotransmitters, peptides, and nucleotides, activate the distinct receptors. Nonodorant receptors form about one-third of the GPCR repertoire. Although more than 200 non-odorant GPCR have been assigned to specific agonists and functions, about 155 socalled "orphan" GPCR (2) await identification of their physiological relevance. The importance of GPCR in controlling almost every physiological function makes this receptor family the most frequently used target for therapeutic drugs. Therefore, unveiling the function of orphan GPCR is a central issue in academic and industrial research.Among the five structurally different GPCR families (1, 3), the rhodopsin-like receptors form the largest in humans and other vertebrates. The rhodopsin-like family is divided further into subfamilies and groups. The P2Y 12 -like receptor group includes the ADP receptors P2Y 12 and P2Y 13 , the UDP-glucose receptor P2Y 14 , and the orphan receptors GPR87, GPR82, and GPR34 (4). Apart from the ADP receptor P2Y 12 , which has a central role in platelet aggregation and is the therapeutic target of clopidogrel (5, 6), very little is known about the function of the other members of this group.GPR34, an orphan receptor of the P2Y 12 -like receptor group, was first discovered by mining GenBank TM for novel GPCR sequences and homology cloning and has been assigned to the human X chromosome (7,8). Phylogenetic studies revealed that GPR34 has been highly conserved over the past 450 million years of vertebrate evolution, and no GPR34-deficient vertebrate has been identified yet (9). To date, there i...

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Osmotic swelling characteristics of glial cells in the murine hippocampus, cerebellum, and retina in situ

Cited by 49 publications

References 50 publications

Brain edema in acute liver failure and chronic liver disease: Similarities and differences

Brain edema in acute liver failure and chronic liver disease: Similarities and differences

Mechanisms of VEGF- and Glutamate-Induced Inhibition of Osmotic Swelling of Murine Retinal Glial (Müller) Cells: Indications for the Involvement of Vesicular Glutamate Release and Connexin-Mediated ATP Release

Altered Immune Response in Mice Deficient for the G Protein-coupled Receptor GPR34

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