Regulatory Volume Decrease in Neural Precursor Cells: Taurine Efflux and Gene Microarray Analysis

Hernández-Benítez, Reyna; Sedeño-Cortés, Adriana E.; Ramos‐Mandujano, Gerardo; Pasantes‐Morales, Herminia

doi:10.1159/000366399

Cited by 7 publications

(9 citation statements)

References 41 publications

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“…As a vital amino acid, taurine is present in abundant amounts in the neural system [33,34]. Taurine can promote the survival of adult RGCs in a pure culture under serumdeprivation condition [35,36].…”

Section: Discussionmentioning

confidence: 99%

The Vigabatrin Induced Retinal Toxicity is Associated with Photopic Exposure and Taurine Deficiency: An In Vivo Study

Tao

Yang

et al. 2016

Cell Physiol Biochem

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Background/Aims: Retinal toxicity is one of the most commonly discussed and concerning adverse effects of vigabatrin (VGB). The present study explored the relationship between the VGB elicited retinal toxicity, photopic exposure, and taurine deficiency, aiming at screening for risk factors to minimize the adverse effects of VGB. Methods: The effects of VGB on function and morphology of mouse retinas were examined via a series of in vivo tests, including electroretinography (ERG), Spectral domain optical coherence tomography (SD-OCT), and optokinetic testing. Moreover, VGB-treated mice were in addition treated with taurine to verify possible protective effects against retinal toxicity. Results: A close relationship between VGB induced retinal toxicity and light exposure was observed. The VGB-treated mice which were reared in darkness preserved better visual function and retinal architectures as verified by the optokinetic tests, OCT and ERG examinations. The retinal taurine level of the VBG-treated mice which were exposed to light were significantly lower than that of the VBG mice reared in darkness. Furthermore, several in vivo evidence provided by our research confirmed that the VGB induced morphological and functional impairments could be partially alleviated by taurine treatment. The present study showed the retinal toxicity of VGB by in vivo measurements. Conclusion: The VGB induced retinal toxicity is closely associated with photopic exposure and taurine deficiency. Patients who are taking VGB might benefit from minimization of light exposure and dietetic taurine supplements.

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Section: Discussionmentioning

confidence: 99%

The Vigabatrin Induced Retinal Toxicity is Associated with Photopic Exposure and Taurine Deficiency: An In Vivo Study

Tao

Yang

et al. 2016

Cell Physiol Biochem

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“…In our study, the expression levels of Notch 1 and Hes 1, which were examined by Western after the cells were treated with fasudil for 6 h compared with other treatment groups; this increase may be due to the oscillation of Hes 1 expression [20]. NSC differentiation and [33] and cell volume change [34].…”

Section: Discussionmentioning

confidence: 85%

Fasudil Stimulates Neurite Outgrowth and Promotes Differentiation in C17.2 Neural Stem Cells by Modulating Notch Signalling but not Autophagy

Shu

Luo

Zhao

et al. 2015

Cell Physiol Biochem

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Background: Neurite outgrowth is one of the important therapeutic strategies for neuronal plasticity and regeneration in neural disorders. Fasudil is a clinical medication that is used to treat subarachnoid haemorrhage (SAH) and that is beneficial for many animal models of central nervous system (CNS) diseases. In this study, we hypothesised that fasudil administration would promote neurite outgrowth in neural stem cells (NSCs). Methods: Changes in cell morphology were imaged under a light microscope, and neurite-bearing cells were counted. Cell viability and the necrosis rate were determined by MTT and LDH assays, respectively. Additionally, western blot and immunofluorescence analyses were performed to detect protein expression levels. Results: We found that fasudil promoted neurite outgrowth in C17.2 cells in a time- and dose-dependent manner. The neurite-bearing C17.2 cells were differentiated by detecting the changes in neural and astrocytic markers after fasudil treatment through down-regulating Notch signalling. Previously, fasudil was reported to induce autophagy, which plays an important role in neural differentiation. However, both rapamycin, an autophagy inducer, and 3-methyl-adenine (3-MA), an autophagy inhibitor, had no effects on the fasudil-induced neurite outgrowth, suggesting that autophagy may be not involved in this process. Conclusion: In summary, fasudil could stimulate neurite outgrowth and differentiation in C17.2 cells by modulating Notch signalling but not autophagy.

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“…Table 1 provides an overview of aquaporin isoform expression by brain cell type [10,56,57,[84][85][86][87][88][89][90]. Astrocytes swell with hypoosmolality and shrink with hyperosmolality within seconds, while most neurons do not [2,7,16]. Neurons resist osmotic swelling (Figs.…”

Section: Sd Is the Common Cause Of Acute Neuronal Swellingmentioning

confidence: 99%

Neuronal Swelling: A Non-osmotic Consequence of Spreading Depolarization

Hellas

Andrew

2021

Neurocrit Care

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An acute reduction in plasma osmolality causes rapid uptake of water by astrocytes but not by neurons, whereas both cell types swell as a consequence of lost blood flow (ischemia). Either hypoosmolality or ischemia can displace the brain downwards, potentially causing death. However, these disorders are fundamentally different at the cellular level. Astrocytes osmotically swell or shrink because they express functional water channels (aquaporins), whereas neurons lack functional aquaporins and thus maintain their volume. Yet both neurons and astrocytes immediately swell when blood flow to the brain is compromised (cytotoxic edema) as following stroke onset, sudden cardiac arrest, or traumatic brain injury. In each situation, neuronal swelling is the direct result of spreading depolarization (SD) generated when the ATP-dependent sodium/potassium ATPase (the Na+/K+ pump) is compromised. The simple, and incorrect, textbook explanation for neuronal swelling is that increased Na+ influx passively draws Cl− into the cell, with water following by osmosis via some unknown conduit. We first review the strong evidence that mammalian neurons resist volume change during acute osmotic stress. We then contrast this with their dramatic swelling during ischemia. Counter-intuitively, recent research argues that ischemic swelling of neurons is non-osmotic, involving ion/water cotransporters as well as at least one known amino acid water pump. While incompletely understood, these mechanisms argue against the dogma that neuronal swelling involves water uptake driven by an osmotic gradient with aquaporins as the conduit. Promoting clinical recovery from neuronal cytotoxic edema evoked by spreading depolarizations requires a far better understanding of molecular water pumps and ion/water cotransporters that act to rebalance water shifts during brain ischemia.

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Regulatory Volume Decrease in Neural Precursor Cells: Taurine Efflux and Gene Microarray Analysis

Cited by 7 publications

References 41 publications

The Vigabatrin Induced Retinal Toxicity is Associated with Photopic Exposure and Taurine Deficiency: An In Vivo Study

The Vigabatrin Induced Retinal Toxicity is Associated with Photopic Exposure and Taurine Deficiency: An In Vivo Study

Fasudil Stimulates Neurite Outgrowth and Promotes Differentiation in C17.2 Neural Stem Cells by Modulating Notch Signalling but not Autophagy

Neuronal Swelling: A Non-osmotic Consequence of Spreading Depolarization

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