Aquaporin-4 expression is not elevated in mild hydrocephalus

Aghayev, Kamran; Bal, Ercan; Rahimli, Tural; Mut, Melike; Balcı, Serdar; Vrionis, Frank D.; Akalan, Nejat

doi:10.1007/s00701-011-1241-9

Cited by 17 publications

(8 citation statements)

References 36 publications

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“…Several descriptive expression studies in hy-drocephalus provide indirect evidence for a role of AQP4 in hydrocephalus. Though no change in brain AQP4 expression was reported in a rat model of mild hydrocephalus produced by kaolin injection [23] , other rat kaolin model studies reported greatly increased AQP4 expression [24] or complex time-and region-dependent alterations in AQP4 expression [25] . Increased AQP4 expression was found in congenital hydrocephalic Texas rats [9] , in dogs with idiopathic communicating internal hydrocephalus [26] , and in a rat model of inflammatory communicating hydrocephalus in which AQP4 expression correlated with the severity of hydrocephalus [27] .…”

Section: Aqp4 and Hydrocephalusmentioning

confidence: 99%

Aquaporin Water Channels and Hydrocephalus

Tradtrantip¹,

Smith²,

Yao³

2016

Pediatr Neurosurg

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The aquaporins (AQPs) are a family of water-transporting proteins that are broadly expressed in mammalian cells. Two AQPs in the central nervous system, AQP1 and AQP4, might play a role in hydrocephalus and are thus potential drug targets. AQP1 is expressed in the ventricular-facing membrane of choroid plexus epithelial cells, where it facilitates the secretion of cerebrospinal fluid (CSF). AQP4 is expressed in astrocyte foot processes and ependymal cells lining ventricles, where it appears to facilitate the transport of excess water out of the brain. Altered expression of these AQPs in experimental animal models of hydrocephalus and limited human specimens suggests their involvement in the pathophysiology of hydrocephalus, as do data in knockout mice demonstrating a protective effect of AQP1 deletion and a deleterious effect of AQP4 deletion in hydrocephalus. Though significant questions remain, including the precise contribution of AQP1 to CSF secretion in humans and the mechanisms by which AQP4 facilitates clearance of excess brain water, AQP1 and AQP4 have been proposed as potential drug targets to reduce ventricular enlargement in hydrocephalus.

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Section: Aqp4 and Hydrocephalusmentioning

confidence: 99%

Aquaporin Water Channels and Hydrocephalus

Tradtrantip¹,

Smith²,

Yao³

2016

Pediatr Neurosurg

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“…AQP4 can facilitate water passing from ventricles into brain parenchyma and then to the systemic circulation [ 1 ]. Whether the disturbance in AQP4 is contributes to hydrocephalus or is protective remains unclear.…”

Section: Discussionmentioning

confidence: 99%

“…Hydrocephalus is a central nervous system disorder that is commonly due to an imbalance between cerebrospinal fluid production and absorption. Excessive accumulation of cerebrospinal fluid leads to ventriculomegaly, increased intracranial pressure, and impaired neuronal functions [ 1 ]. At present, shunting is the main therapeutic method for treating hydrocephalus, but it has a high failure rate.…”

Section: Introductionmentioning

confidence: 99%

Aquaporin 4 Silencing Aggravates Hydrocephalus Induced by Injection of Autologous Blood in Rats

Guo

Zhan

et al. 2018

Med Sci Monit

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BackgroundAquaporin 4 (AQP4), the most abundant aquaporin in the brain, is a type of bidirectional water channel controlling the brain-water balance and plays a critical role in physiologic and pathologic water balance in the brain. AQP4 was reported to be elevated in hydrocephalus; therefore, we hypothesized that AQP4 contributes to hydrocephalus. In this study, the role of AQP4 in hydrocephalus was explored.Material/MethodsThe hydrocephalus rat model was established by injection of autologous blood. On Day 1 and Day 3 after injection of autologous blood, magnetic resonance imaging (MRI) and hematoxylin-eosin (HE) staining were performed to detect the changes in ventricles, and quantitative real-time PCR (qRT-PCR) and immunohistochemistry were carried out to detect the changes in AQP4 level. Thereafter, an AQP4-specific siRNA was used to downregulate AQP4. Then, on Day 3 after injection of autologous blood, the levels of AQP4 and connexin-43 were detected by qRT-PCR, immunohistochemistry, immunofluorescence, or Western blot analysis. MRI and HE staining were performed to detect the changes in ventricles, and Evans blue extravasation assay was used to assess blood-brain barrier integrity.ResultsThe hydrocephalus rat model was established successfully, and hydrocephalus rats showed a higher AQP4 level. Silencing AQP4 aggravated the hydrocephalus, with enlarged lateral ventricles and destruction of ependymal integrity and blood-brain barrier.ConclusionsOur study demonstrates that silencing AQP4 aggravates hydrocephalus, indicating that AQP4 protects against hydrocephalus.

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“…Even though there are quite a lot of aquaporins (water channel proteins) expressed in the CNS, Aquaporin 4 (AQP4) is the major one in the brain, and is expressed in astroglial end feet around the surface of capillaries related to the BBB, glia limitans, and ependyma [ 93 , 94 ]. IS induces both immediate and delayed cell death, which is accompanied by a robust inflammatory response and cerebral edema that can exacerbate injury during reperfusion [ 94 , 95 ].…”

Section: Hmgb1 and Edema Formation In Ismentioning

confidence: 99%

“…Brain edema is the main cause of death in patients with large infarction. AQP4, a water channel protein, is predominantly located in astroglial end feet [ 93 , 94 ] and has been shown to play an important role in water transport in the brain [ 94 , 96 ]. Also, AQP4 is considered to contribute to brain edema, particularly as AQP4-deficient mice have improved outcome following focal ischemic injury [ 94 , 97 ].…”

Section: Hmgb1 and Edema Formation In Ismentioning

confidence: 99%

Pivotal neuroinflammatory and therapeutic role of high mobility group box 1 in ischemic stroke

Richard

Sackey²,

et al. 2017

Bioscience Reports

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Stroke is a major cause of mortality and disability worldwide. Stroke is a frequent and severe neurovascular disorder. The main cause of stroke is atherosclerosis, and the most common risk factor for atherosclerosis is hypertension. Therefore, prevention and treatment of stroke are crucial issues in humans. High mobility group box 1 (HMGB1) is non-histone nuclear protein that is currently one of the crucial proinflammatory alarmins in ischemic stroke (IS). It is instantly released from necrotic cells in the ischemic core and activates an early inflammatory response. HMGB1 may signal via its putative receptors, such as receptor for advanced glycation end products (RAGE), toll-like receptors (TLRs) as well as matrix metalloproteinase (MMP) enzymes during IS. These receptors are expressed in brain cells. Additionally, brain-released HMGB1 can be redox modified in the circulation and activate peripheral immune cells. The role of HMGB1 may be more complex. HMGB1 possesses beneficial actions, such as endothelial activation, enhancement of neurite outgrowth, and neuronal survival. HMGB1 may also provide a novel link for brain-immune communication leading to post-stroke immunomodulation. Therefore, HMGB1 is new promising therapeutic intervention aimed at promoting neurovascular repair and remodeling after stroke. In this review, we look at the mechanisms of secretion of HMGB1, the role of receptors, MMP enzymes, hypoglycemia, atherosclerosis, edema, angiogenesis as well as neuroimmunological reactions and post-ischemic brain recovery in IS. We also outline therapeutic roles of HMGB1 in IS.

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Aquaporin-4 expression is not elevated in mild hydrocephalus

Abstract: Our results indicate that aqp-4 is not up-regulated during the initial stages of hydrocephalus. This implies that aqp-4 may not play a significant role in hydrocephalus compensation until severe ventricular dilatation occurs.

Cited by 17 publications

References 36 publications

Aquaporin Water Channels and Hydrocephalus

Aquaporin Water Channels and Hydrocephalus

Aquaporin 4 Silencing Aggravates Hydrocephalus Induced by Injection of Autologous Blood in Rats

Pivotal neuroinflammatory and therapeutic role of high mobility group box 1 in ischemic stroke

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