The modulation of aquaporin-4 by using PKC-activator (phorbol myristate acetate) and V1a receptor antagonist (SR49059) following middle cerebral artery occlusion/reperfusion in the rat

Okuno, Kenji; Taya, Keisuke; Marmarou, Christina R.; Özişik, Pınar; Fazzina, Giovanna; Kleindienst, Andrea; Gülşen, Salih; Marmarou, Anthony

doi:10.1007/978-3-211-85578-2_84

Cited by 36 publications

(21 citation statements)

References 25 publications

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“…30,40 Importantly, these studies showed a clear correlation between the time course of the traumainduced shift in intracerebral Na + concentrations and the increase in percent brain water content. 22,30,31,39,41 Our findings were consistent with previous reports demonstrating similar shifts between water and Na + content. 31 These data provide a conceptual framework to explain the pathophysiology of cellular swelling that we demonstrate is intimately linked to trauma induced ionic dysfunction, whereas a decrease in extracellular Na + ([Na + ] e ) and a concomitant increase in K + ([K + ] e ) concentrations creates the osmotic gradient that drives water flow into the intracellular compartment, thereby setting the stage for increased brain edema and raised ICP.…”

Section: Introductionsupporting

confidence: 93%

“…Further, experimental models of intracerebral hemorrhage, middle cerebral artery occlusion, ischemia, and cold and traumatic brain injury have demonstrated that V1aR inhibition reduces brain edema. [22][23][24][25][26][27][28][29][30][31] The underlying mechanism of this response has been attributed to either modulation of vasopressin in the brain parenchyma 17 or its interaction with aquaporin-4 (AQP4). AQP4 is the predominant water channel in the brain and has a significant role in the pathophysiology of brain edema.…”

Section: Introductionmentioning

confidence: 99%

“…[32][33][34][35][36] Evidence suggests V1aR regulate the expression and function of AQP4, 17,22,37 although the mechanism is still elusive. 17,22,[29][30][31] Recently, we explored the hypothesis that selective V1aR inhibition by the non-peptide antagonist SR49059 30,38 can reduce brain edema in animal models of middle cerebral artery occlusion 22,39 and TBI. 30 Overall, we showed that V1aR inhibition decreases brain AQP4 expression, brain edema, and astrocytic cell swelling, and reduces expression of V1aR.…”

Section: Introductionmentioning

confidence: 99%

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Real-Time Monitoring of Changes in Brain Extracellular Sodium and Potassium Concentrations and Intracranial Pressure after Selective Vasopressin-1a Receptor Inhibition following Focal Traumatic Brain Injury in Rats

Filippidis

Liang²,

Wang³

et al. 2014

Journal of Neurotrauma

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Brain swelling and increased intracranial pressure (ICP) following traumatic brain injury (TBI) contribute to poor outcome. Vasopressin-1a receptors (V1aR) and aquaporin-4 (AQP4) regulate water transport and brain edema formation, perhaps in part by modulating cation fluxes. After focal TBI, V1aR inhibitors diminish V1aR and AQP4, reduce astrocytic swelling and brain edema. We determined whether V1aR inhibition with SR49059 after lateral controlled-cortical-impact (CCI) injury affects extracellular Na. Ion-selective Na + and K + electrodes (ISE) and an ICP probe were implanted in rat parietal cortex, and [Na + ] e , [K + ] e , and physiological parameters were monitored for 5 h post-CCI. Sham-vehicle-ISE, CCI-vehicle-ISE and CCI-SR49059-ISE groups were studied, and SR49059 was administered 5 min to 5 h post-injury. We found a significant injury-induced decrease in [Na + ] e to 80.1 -15 and 87.9 -7.9 mM and increase in [K + ] e to 20.9 -3.8 and 13.4 -3.4 mM at 5 min post-CCI in CCI-vehicle-ISE and CCI-SR49059-ISE groups, respectively (p < 0.001 vs. baseline; ns between groups). Importantly, [Na + ] e in CCI-SR49059-ISE was reduced 5-20 min post-injury and increased to baseline at 25 min, whereas recovery in CCI-vehicle-ISE required more than 1 hr, suggesting SR49059 accelerated [Na + ] e recovery. In contrast, [K + ] e recovery took 45 min in both groups. Further, ICP was lower in the CCI-SR49059-ISE group. Thus, selective V1aR inhibition allowed faster [Na + ] e recovery and reduced ICP. By augmenting the [Na + ] e recovery rate, SR49059 may reduce trauma-induced ionic imbalance, blunting cellular water influx and edema after TBI. These findings suggest SR49059 and V1aR inhibitors are potential tools for treating cellular edema post-TBI.

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Section: Introductionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Real-Time Monitoring of Changes in Brain Extracellular Sodium and Potassium Concentrations and Intracranial Pressure after Selective Vasopressin-1a Receptor Inhibition following Focal Traumatic Brain Injury in Rats

Filippidis

Liang²,

Wang³

et al. 2014

Journal of Neurotrauma

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“…It should be noted that a part of the intracranial artery causes vasodilatation upon AVP stimulation in an endothelium-dependent manner (264,386 Cerebral edema is a devastating consequence of brain injury that leads to compromised cerebral blood flow and worsening parenchymal damage. Blockade of the V1a receptor by SR49059 has been shown to significantly reduce intracranial pressure or cerebral edema after cortical contusion injury, intracerebral hemorrhage injury, or cerebral artery occlusion in animal models (275,322,384,457,487). Likewise, the V1a/V2 receptor antagonist YM087 (conivaptan) significantly reduced intracranial pressure and cerebral edema after traumatic brain injury (122,168).…”

Section: Cerebral Vasospasm and Brain Edemamentioning

confidence: 99%

Vasopressin V1a and V1b Receptors: From Molecules to Physiological Systems

Koshimizu

Nakamura

Egashira

et al. 2012

Physiological Reviews

324

297

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The neurohypophysial hormone arginine vasopressin (AVP) is essential for a wide range of physiological functions, including water reabsorption, cardiovascular homeostasis, hormone secretion, and social behavior. These and other actions of AVP are mediated by at least three distinct receptor subtypes: V1a, V1b, and V2. Although the antidiuretic action of AVP and V2 receptor in renal distal tubules and collecting ducts is relatively well understood, recent years have seen an increasing understanding of the physiological roles of V1a and V1b receptors. The V1a receptor is originally found in the vascular smooth muscle and the V1b receptor in the anterior pituitary. Deletion of V1a or V1b receptor genes in mice revealed that the contributions of these receptors extend far beyond cardiovascular or hormone-secreting functions. Together with extensively developed pharmacological tools, genetically altered rodent models have advanced the understanding of a variety of AVP systems. Our report reviews the findings in this important field by covering a wide range of research, from the molecular physiology of V1a and V1b receptors to studies on whole animals, including gene knockout/knockdown studies.

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“…21) Additionally, previous studies indicate that the expression level of AQPs increase when PKC is activated. [22][23][24] Therefore, the mechanism of the observed increase in AQP3 expression following the addition of Gypsum fibrosum or CaSO 4 was investigated with a focus on the Ca-PKC pathway.…”

Section: Effect Of Gypsum Fibrosum or Caso 4 On The Intracellular Ca mentioning

confidence: 99%

Elucidating the Mechanism by Which <i>Gypsum fibrosum</i>, a Traditional Chinese Medicine, Maintains Cutaneous Water Content

Ikarashi

Ogiue

Toyoda

et al. 2013

Biological & Pharmaceutical Bulletin

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Aquaporin-3 (AQP3) plays an important role in maintaining the normal water content of the skin. Previously, we revealed that the expression of cutaneous AQP3 increased following oral administration of Gypsum fibrosum (main component: CaSO 4 ) to mice. The purpose of this study is to elucidate the mechanism by which Gypsum fibrosum increases the expression of cutaneous AQP3 in a keratinocyte cell line. Gypsum fibrosum or CaSO 4 was added to keratinocytes, and the expression level of AQP3, the Ca concentration, the activity of protein kinase C (PKC), and the degrees of phosphorylation of both extracellular signal-regulated kinase (ERK) and cAMP response element binding protein (CREB) were measured. The mRNA and protein expression levels of AQP3 increased significantly 6 h-post addition of Gypsum fibrosum. In keratinocytes treated with Gypsum fibrosum, increases in the concentration of intracellular Ca, PKC activity, and the phosphorylation of ERK and CREB were observed. Pre-treatment with GF109203X, a PKC inhibitor, suppressed the mRNA expression levels of AQP3. Similarly to treatment with Gypsum fibrosum, the addition of CaSO 4 led to the same observations in keratinocytes. It is hypothesized that Gypsum fibrosum causes an increase in the intracellular Ca concentration, PKC activity, and the phosphorylation levels of ERK and CREB, resulting in increased AQP3 expression in keratinocytes. In addition, it is possible that the effect of Gypsum fibrosum is attributable to CaSO 4 , based on the results demonstrating that the mechanisms of action of Gypsum fibrosum and CaSO 4 were nearly identical.

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The modulation of aquaporin-4 by using PKC-activator (phorbol myristate acetate) and V1a receptor antagonist (SR49059) following middle cerebral artery occlusion/reperfusion in the rat

Cited by 36 publications

References 25 publications

Real-Time Monitoring of Changes in Brain Extracellular Sodium and Potassium Concentrations and Intracranial Pressure after Selective Vasopressin-1a Receptor Inhibition following Focal Traumatic Brain Injury in Rats

Real-Time Monitoring of Changes in Brain Extracellular Sodium and Potassium Concentrations and Intracranial Pressure after Selective Vasopressin-1a Receptor Inhibition following Focal Traumatic Brain Injury in Rats

Vasopressin V1a and V1b Receptors: From Molecules to Physiological Systems

Elucidating the Mechanism by Which <i>Gypsum fibrosum</i>, a Traditional Chinese Medicine, Maintains Cutaneous Water Content

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