Aquaporins and Glia

Albertini, Roberta; Bianchi, Rossella

doi:10.2174/157015910791233178

Cited by 27 publications

(11 citation statements)

References 106 publications

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“…AQP4 is the major aquaporin form expressed in brain, and primarily in astroglia (Gunnarson et al, 2004); activated microglia also express AQP4 in some studies but not others (Li et al, 2011; Tomas-Camardiel et al, 2004). Increased brain AQP4 levels and activity are important mediators of cytotoxic (cellular) edema in acquired neurodegenerative conditions such as ischemia, stroke and trauma (Roberta and Rossella, 2010; Saadoun and Papadopoulos, 2010). In that regard, moderate brain edema is present in repetitive binge ethanol-treated adult rats and organotypic HC+EC slice cultures, and is reduced by an AQP4 inhibitor (Collins et al, 1998; Sripathirathan et al, 2009).…”

Section: Discussionmentioning

confidence: 99%

Effect of repetitive daily ethanol intoxication on adult rat brain: Significant changes in phospholipase A2 enzyme levels in association with increased PARP-1 indicate neuroinflammatory pathway activation

Tajuddin

Przybycien-Szymanska

Pak

et al. 2013

Alcohol

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Collaborating on studies of subchronic daily intoxication in juvenile and adult rats, we examined whether the repetitive ethanol treatments at these two life stages altered levels of key neuroinflammation-associated proteins—aquaporin-4 (AQP4), certain phospholipase A2 (PLA2) enzymes, PARP-1 and caspase-3—in hippocampus (HC) and entorhinal cortex (EC). Significant changes in the proteins could implicate activation of specific neuroinflammatory signaling pathways in these rats as well as in severely binge-intoxicated adult animals that are reported to incur degeneration of vulnerable neurons in HC and EC. Male Wistar rats, ethanol-intoxicated (3 g/kg i.p.) once daily for 6 days over an 8-day interval beginning at 37 days old and repeated at age 68–75 days, were sacrificed one hr after the day 75 dose (blood ethanol, 200–230 mg/dl). Analysis of HC with an immunoblot technique showed that AQP4, Ca+2-dependent PLA2 (cPLA2 IVA), phosphorylated (activated) p-cPLA2, cleaved (89 kD) PARP (c-PARP), and caspase-3 levels were significantly elevated over controls, whereas Ca+2-independent PLA2 (iPLA2 VIA) was reduced ~70%; however, cleaved caspase-3 was undetectable. In the EC, AQP4 was unchanged, but cPLA2 and p-cPLA2 were significantly increased while iPLA2 levels were diminished (~40%) similar to HC, although just outside statistical significance (p=0.06). In addition, EC levels of PARP-1 and c-PARP were significantly increased. The ethanol-induced activation of cPLA2 in association with reduced iPLA2 mirrors PLA2 changes in reports of neurotrauma and also of dietary omega-3 fatty acid depletion. Furthermore, the robust PARP-1 elevations accompanied by negligible caspase-3 activation indicate that repetitive ethanol intoxication may be potentiating non-apoptotic neurodegenerative processes such as parthanatos. Overall, the repetitive ethanol treatments appeared to instigate previously unappreciated neuroinflammatory pathways in vivo. The data provide insights into mechanisms of binge ethanol abuse that might suggest new therapeutic approaches to counter neurodegeneration and dementia.

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Section: Discussionmentioning

confidence: 99%

Effect of repetitive daily ethanol intoxication on adult rat brain: Significant changes in phospholipase A2 enzyme levels in association with increased PARP-1 indicate neuroinflammatory pathway activation

Tajuddin

Przybycien-Szymanska

Pak

et al. 2013

Alcohol

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“…The red line represents the calculated IC 50 value. (Albertini and Bianchi, 2010;Badaut et al, 2012;Potokar et al, 2016). Moreover, silencing of AQP9 in murine astrocytes decreased glycerol uptake and increased glucose and oxidative metabolism, suggesting its importance for astrocyte metabolism (Badaut et al, 2012).…”

Section: Inflammatory Scenariomentioning

confidence: 98%

“…Moreover, this enzyme has been associated with working memory performance in young adults (Greenwood et al, 2018). On the other hand, six isoforms of aquaporins (AQP 1,3,4,5,8,9) have been reported in glial cells, performing important functions like water transport, regulation of the cerebrospinal fluid (CSF), synaptic remodeling, formation of brain edemas and inflammatory processes (Saparov et al, 2007;Te Velde et al, 2008;Albertini and Bianchi, 2010;Nagahara et al, 2010). Aquaporin 9 (AQP9) is highly expressed in the inner mitochondrial membrane of astrocytes (Potokar et al, 2016).…”

Section: Inflammatory Scenariomentioning

confidence: 99%

Multiple Pathways Involved in Palmitic Acid-Induced Toxicity: A System Biology Approach

et al. 2020

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Inflammation is a complex biological response to injuries, metabolic disorders or infections. In the brain, astrocytes play an important role in the inflammatory processes during neurodegenerative diseases. Recent studies have shown that the increase of free saturated fatty acids such as palmitic acid produces a metabolic inflammatory response in astrocytes generally associated with damaging mechanisms such as oxidative stress, endoplasmic reticulum stress, and autophagic defects. In this aspect, the synthetic neurosteroid tibolone has shown to exert protective functions against inflammation in neuronal experimental models without the tumorigenic effects exerted by sexual hormones such as estradiol and progesterone. However, there is little information regarding the specific mechanisms of tibolone in astrocytes during inflammatory insults. In the present study, we performed a genome-scale metabolic reconstruction of astrocytes that was used to study astrocytic response during an inflammatory insult by palmitate through Flux Balance Analysis methods and data mining. In this aspect, we assessed the metabolic fluxes of human astrocytes under three different scenarios: healthy (normal conditions), induced inflammation by palmitate, and tibolone treatment under palmitate inflammation. Our results suggest that tibolone reduces the L-glutamate-mediated neurotoxicity in astrocytes through the modulation of several metabolic pathways involved in glutamate uptake. We also identified a set of reactions associated with the protective effects of tibolone, including the upregulation of taurine metabolism, gluconeogenesis, cPPAR and the modulation of calcium signaling pathways. In conclusion, the different scenarios studied in our model allowed us to identify several metabolic fluxes perturbed under an inflammatory response and the protective mechanisms exerted by tibolone.

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“…Co-localisation of AQP4 and the Kir4.1 has been demonstrated in retinal Muller cells by EM immunogold labelling [26] and co-immunoprecipitation [27]. The partnership facilitates K + siphoning within the central nervous system to clear excess potassium around active neurones [8]. Water transport in this setting controls neural signal transduction.…”

Section: Protein Partnersmentioning

confidence: 97%

“…Non-endfeet membranes within the neuropil also contain a low density of AQP4. This subcellular compartmentalisation facilitates redistribution of water between the extracellular space and vascular or ventricular compartments [8].…”

mentioning

confidence: 99%