Central Role of Maladapted Astrocytic Plasticity in Ischemic Brain Edema Formation

Wang, Yufeng; Parpura, Vladimir

doi:10.3389/fncel.2016.00129

Cited by 53 publications

(70 citation statements)

References 82 publications

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“…The cytotoxic cerebral edema may result from disruption in cellular metabolism and the subsequent cellular retention of Na + and water due to poisoning or hypoxia. Hypoxia‐associated cytotoxic cerebral edema is typically observed in ischemic cerebral stroke (Jia, Liu, Wang, & Wang, ), in which astrocytes are a critical contributor (Wang & Parpura, ). The swelling can impose pressure on normal brain structures and thus causes atrophy or herniation.…”

Section: Gfap and Neurological Diseasesmentioning

confidence: 99%

“…Another aftermath of the astrocytic swelling is the occurrence of abnormal RVD. During RVD, astrocytes release organic osmolytes and neurotoxic substances that could cause inflammation (Cavet, Harrington, Vollmer, Ward, & Zhang, ), a hyperosmotic environment (Wang & Parpura, ), and astrocytic apoptosis and neurodegeneration (Ben Messaoud, Katzarova, & Lopez, ), thereby leading to irreversible brain damage.…”

Section: Gfap and Neurological Diseasesmentioning

confidence: 99%

“…Nevertheless, GFAP‐associated changes in astrocytic morphology can further alter interneuronal junctional communication, synaptic innervations, cellular apposition as well as astrocytic uptaking extracellular glutamate, K + , and other chemicals. These indirect functions of GFAP have been reviewed extensively (Wang & Hamilton, ; Wang & Parpura, ; Wang & Zhu, ) and are not further extended here.…”

Section: Gfap Functionsmentioning

confidence: 99%

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Neurochemical regulation of the expression and function of glial fibrillary acidic protein in astrocytes

Liu

et al. 2019

Glia

117

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Glial fibrillary acidic protein (GFAP), a type III intermediate filament, is a marker of mature astrocytes. The expression of GFAP gene is regulated by many transcription factors (TFs), mainly Janus kinase‐2/signal transducer and activator of transcription 3 cascade and nuclear factor κ‐light‐chain‐enhancer of activated B cell signaling. GFAP expression is also modulated by protein kinase and other signaling molecules that are elicited by neuronal activity and hormones. Abnormal expression of GFAP proteins occurs in neuroinflammation, neurodegeneration, brain edema‐eliciting diseases, traumatic brain injury, psychiatric disorders and others. GFAP, mainly in α‐isoform, is the major component of cytoskeleton and the scaffold of astrocytes, which is essential for the maintenance of astrocytic structure and shape. GFAP also has highly morphological plasticity because of its quick changes in assembling and polymerizing states in response to environmental challenges. This plasticity and its corresponding cellular morphological changes endow astrocytes the functions of physical barrier between adjacent neurons and stabilizer of extracellular environment. Moreover, GFAP colocalizes and even molecularly associates with many functional molecules. This feature allows GFAP to function as a platform for direct interactions between different molecules. Last, GFAP involves transportation and localization of other functional proteins and thus serves as a protein transport guide in astrocytes. This guiding role of GFAP involves an elastic retraction and extension cytoskeletal network that couples with GFAP reassembling, transporting, and membrane protein recycling machinery. This paper reviews our current understanding of the expression and functions of GFAP as well as their regulation.

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Section: Gfap and Neurological Diseasesmentioning

confidence: 99%

Section: Gfap and Neurological Diseasesmentioning

confidence: 99%

Section: Gfap Functionsmentioning

confidence: 99%

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Neurochemical regulation of the expression and function of glial fibrillary acidic protein in astrocytes

Liu

et al. 2019

Glia

117

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“…Reactive gliosis and the formation of glial scar provide a way of containing and initiating the repair process (Liddelow & Barres, ). Astrocyte reactivity is important in regulating the neurovasculature when the blood brain barrier is at risk and this becomes highly relevant in neurodegenerative and traumatic injuries (Wang & Parpura, ). In response to signaling molecules from the damage site, oligodendrocytes respond to the area and begin remyelinating (Carmen et al, 2007).…”

Section: Reactive Gliosismentioning

confidence: 99%

TSPO regulation in reactive gliotic diseases

McNeela

Bernick

Hines

et al. 2018

J of Neuroscience Research

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The brain is the most metabolically active organ in the body. This high metabolic demand is apparent in that 60% of the brain is comprised of mitochondria-enriched cells. A disruption of the brain's ability to meet this immense metabolic demand is central to the pathogenesis of a multitude of neurological disorders, which range from depression to Alzheimer's disease. Central to these pathologies are glial signaling and energy metabolism cascades regulating apoptosis and inflammation. Thus, diseases causing inflammation and disruption of metabolism can be correlated with glial reactivity. Acutely, reactive gliosis provides a mechanism for limiting the progression of a disease. Following chronic activation, the ability of reactive gliosis to limit disease progression decreases and, in some cases, transitions into a harmful state. The necessity for a noninvasive biomarker of disease in the brain has linked reactive gliosis with an upregulation of translocator protein (TSPO). TSPO is an 18kDa protein that is both a therapeutic target for multiple acute and chronic neuroinflammatory diseases and the leading biomarker for Alzheimer's disease. Although a central function of TSPO is not well known, the protein was named for its ability to translocate cholesterol. Increased TSPO expression is an indicator of disrupted metabolic activity and increased reactive oxygen production. The changes in TSPO expression levels both temporally and spatially relate to the pathogenesis of stroke, Alzheimer's disease, traumatic brain injury, and depression. Therefore, research into the basic function and potential therapeutics targeting TSPO will have broad implications for many diseases of the brain.

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“…Importantly, astrocytes can influence neuronal activity through multiple approaches (Wang and Zhu, 2014; Hertz and Chen, 2016; Wang and Parpura, 2016). For instance, β-alanine release from astrocytes (Pasantes-Morales et al, 1994) can inhibit astrocyte GABA transporters and thus inhibits VP secretion through increasing extracellular GABA (Wang et al, 2013a); coordinated D-serine metabolism between astrocytes and magnocellular neurons along with exhaustion of β-alanine and taurine in the SON can increase NMDA receptor activation, and participate in the recovery of VP neurons from hyposmotic inhibition (Wang et al, 2013b).…”

Section: Cellular Volumementioning

confidence: 99%

Interactions of the Mechanosensitive Channels with Extracellular Matrix, Integrins, and Cytoskeletal Network in Osmosensation

Jiao

Cui

Wang

et al. 2017

Front. Mol. Neurosci.

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Life is maintained in a sea water-like internal environment. The homeostasis of this environment is dependent on osmosensory system translation of hydromineral information into osmotic regulatory machinery at system, tissue and cell levels. In the osmosensation, hydromineral information can be converted into cellular reactions through osmoreceptors, which changes thirst and drinking, secretion of antidiuretic vasopressin (VP), reabsorption of water and salt in the kidneys at systemic level as well as cellular metabolic activity and survival status at tissue level. The key feature of osmosensation is the activation of mechanoreceptors or mechanosensors, particularly transient receptor potential vallinoid (TRPV) and canonical (TRPC) family channels, which increases cytosolic Ca2+ levels, activates osmosensory cells including VP neurons and triggers a series of secondary reactions. TRPV channels are sensitive to both hyperosmotic and hyposmotic stimuli while TRPC channels are more sensitive to hyposmotic challenge in neurons. The activation of TRP channels relies on changes in cell volume, membrane stretch and cytoskeletal reorganization as well as hydration status of extracellular matrix (ECM) and activity of integrins. Different families of TRP channels could be activated differently in response to hyperosmotic and hyposmotic stimuli in different spatiotemporal orders, leading to differential reactions of osmosensory cells. Together, they constitute the osmosensory machinery. The activation of this osmoreceptor complex is also associated with the activity of other osmolarity-regulating organelles, such as water channel protein aquaporins, Na-K-2Cl cotransporters, volume-sensitive anion channels, sodium pump and purinergic receptors in addition to intercellular interactions, typically astrocytic neuronal interactions. In this article, we review our current understandings of the composition of osmoreceptors and the processes of osmosensation.

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Central Role of Maladapted Astrocytic Plasticity in Ischemic Brain Edema Formation

Cited by 53 publications

References 82 publications

Neurochemical regulation of the expression and function of glial fibrillary acidic protein in astrocytes

Neurochemical regulation of the expression and function of glial fibrillary acidic protein in astrocytes

TSPO regulation in reactive gliotic diseases

Interactions of the Mechanosensitive Channels with Extracellular Matrix, Integrins, and Cytoskeletal Network in Osmosensation

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