Role of aquaporin-4 in the development of brain oedema in liver failure

Wright, Gavin; Soper, Robin; Brooks, Heather F.; Stadlbauer, Vanessa; Vairappan, Balasubramaniyan; Davies, Nathan; Andreola, Fausto; Hodges, Stephen; Moss, R.E.; Davies, D.C.; Jalan, Rajiv

doi:10.1016/j.jhep.2010.02.020

Cited by 55 publications

(40 citation statements)

References 54 publications

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“…An increase of Aqp-4 expression has been found in ammoniainduced swelling of cultured astrocytes (Rama Rao et al, 2003). Furthermore, an increase in expression of Aqp-4 in the brain, in association with brain edema, has been demonstrated in both ALF mice (Eefsen et al, 2010) and cirrhotic rats (Wright et al, 2010). However, on the contrary, the presence of brain edema was not related with an increase in brain Aqp-4 in either galactosamine treated or chronic hyperammonemic (induced by hyperammonemic diet) rats (Wright et al, 2010).…”

Section: Water Channelsmentioning

confidence: 98%

“…Furthermore, an increase in expression of Aqp-4 in the brain, in association with brain edema, has been demonstrated in both ALF mice (Eefsen et al, 2010) and cirrhotic rats (Wright et al, 2010). However, on the contrary, the presence of brain edema was not related with an increase in brain Aqp-4 in either galactosamine treated or chronic hyperammonemic (induced by hyperammonemic diet) rats (Wright et al, 2010). Therefore, inconsistent results relating the upregulation of Aqp-4 with brain edema dictate future investigations.…”

Section: Water Channelsmentioning

confidence: 99%

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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: Water Channelsmentioning

confidence: 98%

Section: Water Channelsmentioning

confidence: 99%

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

Bosoi

Rose

2013

Neurochemistry International

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“…An increase in plasma bilirubin levels is a common result of BDL that has been widely reported across literatures (Adler et al 1977;Maillette de Buy Wenniger and Beuers 2010;Rodriguez-Garay 2003). The increased levels of bilirubin in plasma confirmed obstruction of common bile duct during the surgical laparotomy, which in turn might cause chronic liver failure (Butterworth et al 2009;Magen et al 2009;Wright et al 2010). In addition, chronic liver failure may induce hyperammonemia and HE, which has been previously reported by other investigators (Cauli et al 2009a;Rodrigo et al 2010).…”

Section: Discussionmentioning

confidence: 86%

Hepatic encephalopathy induces site-specific changes in gene expression of GluN1 subunit of NMDA receptor in rat brain

2015

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We investigate changes in gene expression of GluN1 subunit of N-Methyl-D-Aspartate (NMDA) receptor in the prefrontal cortex (PFC), hippocampus and striatum in a rat model of hepatic encephalopathy (HE). We used male Wistar rats in which HE was induced after a common bile duct ligation (BDL). The animals were divided into three sets, and each set included three groups of control, sham operated and BDL. In the first set of animals, blood samples collected for biochemical analysis on day 21 of BDL. In the second set, changes in nociception threshold was assessed on day 21 of BDL using a hotplate test. In the third set, whole brain extracted, and the PFC, the hippocampus and the striatum in each rat were immediately dissected. We used a semi-quantitative RT-PCR method for evaluating the GluN1 gene expression. The biochemical analyses showed that plasma levels of ammonia and bilirubin in BDL rats were significantly increased compared to the sham control group on day 21 of BDL (P < 0.01). Nociception threshold was also increased in rats with BDL compared to sham group (P < 0.001). The results revealed that the GluN1 gene expression at mRNA levels in BDL group was decreased by 19 % in the PFC (P < 0.05) but increased by 82 % in the hippocampus (P < 0.01) compared to the sham control group; however, no significant change was observed in the striatum. It can be concluded that HE affects the GluN1 gene expression in rat brain with a site-specific pattern, and the PFC and hippocampus are more sensitive areas than striatum.

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“…It has been shown that the presence of HE grade 3/4 correlates better with inflammation than with ammonia plasma levels (Shawcross, Sharifi et al 2010), though extracellular brain ammonia levels may be significantly higher. One recent study showed that in a cirrhosis animal model in which plasma and brain cytokines were markedly elevated following administration of lipopolysaccharide (LPS), pre-treatment with OP prevented increased levels of TNFα and IL-6 (trend) in plasma and in brain observed in the control group (Wright G 2010). Moreover, OP reduced LPS induced development of pre-coma/coma and worsening of brain edema.…”

Section: Effects Of Ornithinephenylacetate On Glutaminase Activity Inmentioning

confidence: 99%

The Rise of Glutaminase in End-Stage Liver Diseases

Jover-Cobos¹,

Davies²,

Jalan³

et al. 2012

Liver Transplantation - Basic Issues

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Role of aquaporin-4 in the development of brain oedema in liver failure

Cited by 55 publications

References 54 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

Hepatic encephalopathy induces site-specific changes in gene expression of GluN1 subunit of NMDA receptor in rat brain

The Rise of Glutaminase in End-Stage Liver Diseases

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