RETRACTED: Melatonin renders neuroprotection by protein kinase C mediated aquaporin-4 inhibition in animal model of focal cerebral ischemia

Bhattacharya, Pallab; Pandey, Anand Kumar; Sauseng, Paul; Patnaik, Ranjana

doi:10.1016/j.lfs.2014.01.085

Cited by 49 publications

(35 citation statements)

References 72 publications

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“…Zelenina et al (2002) further pointed out that it was through direct phosphorylation of AQP4 at Ser180, rather than an intermediary pathway, that PKC regulated AQP4 water permeability. In addtion, the study with molecular docking and western blot analysis (Bhattacharya et al, 2014) provided an direct evidence that activation of PKC can inhibit the expression of AQP4 and improve the neurological outcome.…”

Section: Discussionmentioning

confidence: 95%

Hydrogen sulfide induces neuroprotection against experimental stroke in rats by down-regulation of AQP4 via activating PKC

et al. 2015

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Section: Discussionmentioning

confidence: 95%

Hydrogen sulfide induces neuroprotection against experimental stroke in rats by down-regulation of AQP4 via activating PKC

et al. 2015

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“…Melatonin administered post-stroke inhibits PKCδ in a rat model, effectively reducing aquaporin-1, brain edema, and infarct size [146]. Curcumin inhibits neuroinflammation by mitigating PKC induced toll-like receptor activation [147].…”

Section: Interrelating Pkc Stroke and Admentioning

confidence: 99%

Common Mechanisms of Alzheimer's Disease and Ischemic Stroke: The Role of Protein Kinase C in the Progression of Age-Related Neurodegeneration

Lucke‐Wold

Turner

Logsdon

et al. 2014

JAD

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Ischemic stroke and Alzheimer’s disease (AD), despite being distinct disease entities, share numerous pathophysiological mechanisms such as those mediated by inflammation, immune exhaustion, and neurovascular unit compromise. An important shared mechanistic link is acute and chronic changes in protein kinase C (PKC) activity. PKC isoforms have widespread functions important for memory, blood-brain barrier maintenance, and injury repair that change as the body ages. Disease states accelerate PKC functional modifications. Mutated forms of PKC can contribute to neurodegeneration and cognitive decline. In some cases the PKC isoforms are still functional but are not successfully translocated to appropriate locations within the cell. The deficits in proper PKC translocation worsen stroke outcome and amyloid-β toxicity. Cross talk between the innate immune system and PKC pathways contribute to the vascular status within the aging brain. Unfortunately, comorbidities such as diabetes, obesity, and hypertension disrupt normal communication between the two systems. The focus of this review is to highlight what is known about PKC function, how isoforms of PKC change with age, and what additional alterations are consequences of stroke and AD. The goal is to highlight future therapeutic targets that can be applied to both the treatment and prevention of neurologic disease. Although the pathology of ischemic stroke and AD are different, the similarity in PKC responses warrants further investigation, especially as PKC-dependent events may serve as an important connection linking age-related brain injury.

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“…It was reported that AQP4 was down-regulated by activating protein kinase C (PKC) pathway by hydrogen sulfide or melatonin after MCAO, suggesting PKC pathway is essential for AQP4 down-regulation [56,57]. Mitogen-activated protein kinase (MAPK) pathways include three main members: extracellular signal-regulated kinase (ERK), C-Jun amino-terminal kinase (JNK) and p38-MAPK.…”

Section: Cerebral Ischemiamentioning

confidence: 99%

Aquaporin-4 and Cerebrovascular Diseases

Chu

Huang

Ding

et al. 2016

IJMS

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Cerebrovascular diseases are conditions caused by problems with brain vasculature, which have a high morbidity and mortality. Aquaporin-4 (AQP4) is the most abundant water channel in the brain and crucial for the formation and resolution of brain edema. Considering brain edema is an important pathophysiological change after stoke, AQP4 is destined to have close relation with cerebrovascular diseases. However, this relation is not limited to brain edema due to other biological effects elicited by AQP4. Till now, multiple studies have investigated roles of AQP4 in cerebrovascular diseases. This review focuses on expression of AQP4 and the effects of AQP4 on brain edema and neural cells injuries in cerebrovascular diseases including cerebral ischemia, intracerebral hemorrhage and subarachnoid hemorrhage. In the current review, we pay more attention to the studies of recent years directly from cerebrovascular diseases animal models or patients, especially those using AQP4 gene knockout mice. This review also elucidates the potential of AQP4as an excellent therapeutic target.

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RETRACTED: Melatonin renders neuroprotection by protein kinase C mediated aquaporin-4 inhibition in animal model of focal cerebral ischemia

Cited by 49 publications

References 72 publications

Hydrogen sulfide induces neuroprotection against experimental stroke in rats by down-regulation of AQP4 via activating PKC

Hydrogen sulfide induces neuroprotection against experimental stroke in rats by down-regulation of AQP4 via activating PKC

Common Mechanisms of Alzheimer's Disease and Ischemic Stroke: The Role of Protein Kinase C in the Progression of Age-Related Neurodegeneration

Aquaporin-4 and Cerebrovascular Diseases

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