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1
Strange, K. "Regulation of solute and water balance and cell volume in the central nervous system." Journal of the American Society of Nephrology 3, no. 1 (July 1992): 12–27. http://dx.doi.org/10.1681/asn.v3112.
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The mammalian brain is composed of four distinct fluid compartments: blood, cerebral spinal fluid, interstitial fluid surrounding glial cells and neurons, and intracellular fluid. Maintenance of the ionic and osmotic composition and volume of these fluids is crucial for the normal functioning of the brain. Small changes in intracellular or extracellular solute composition can dramatically alter neuronal signaling and information processing. Because of the rigid confines of the skull and complex brain architecture, changes in total brain volume can cause devastating neurological damage. As a result, it is not surprising to find that the composition and volume of brain intracellular and extracellular fluids are controlled tightly under both normal conditions and in various disease states. Osmotic and ionic balance in the central nervous system is regulated by solute and water transport across the blood-brain barrier, the choroid plexus, and the plasma membrane of glial cells and neurons. Despite its clinical and physiological significance, however, little is known about the underlying cellular and molecular mechanisms by which the central nervous system's osmotic and ionic balance is maintained. In this review, the current understanding of osmoregulation in the mammalian brain and its role in various disease processes such as hyponatremia, renal failure, and hypernatremia will be summarized. A detailed understanding of brain osmoregulatory processes represents a fundamental physiological problem and is required for the treatment of numerous disease states, particularly those encountered in the practice of nephrology.
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Sun, Dandan, and Sangita G. Murali. "Stimulation of Na+-K+-2Cl−cotransporter in neuronal cells by excitatory neurotransmitter glutamate." American Journal of Physiology-Cell Physiology 275, no. 3 (September 1, 1998): C772—C779. http://dx.doi.org/10.1152/ajpcell.1998.275.3.c772.
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Na+-K+-2Cl−cotransporters are important in renal salt reabsorption and in salt secretion by epithelia. They are also essential in maintenance and regulation of ion gradients and cell volume in both epithelial and nonepithelial cells. Expression of Na+-K+-2Cl−cotransporters in brain tissues is high; however, little is known about their function and regulation in neurons. In this study, we examined regulation of the Na+-K+-2Cl−cotransporter by the excitatory neurotransmitter glutamate. The cotransporter activity in human neuroblastoma SH-SY5Y cells was assessed by bumetanide-sensitive K+ influx, and protein expression was evaluated by Western blot analysis. Glutamate was found to induce a dose- and time-dependent stimulation of Na+-K+-2Cl−cotransporter activity in SH-SY5Y cells. Moreover, both the glutamate ionotropic receptor agonist N-methyl-d-aspartic acid (NMDA) and the metabotropic receptor agonist (±)-1-aminocyclopentane- trans-1,3-dicarboxylic acid ( trans-ACPD) significantly stimulated the cotransport activity in these cells. NMDA-mediated stimulation of the Na+-K+-2Cl−cotransporter was abolished by the selective NMDA-receptor antagonist (+)-MK-801 hydrogen maleate. trans-ACPD-mediated effect on the cotransporter was blocked by the metabotropic receptor antagonist (+)-α-methyl-(4-carboxyphenyl)glycine. The results demonstrate that Na+-K+-2Cl−cotransporters in neurons are regulated by activation of both ionotropic and metabotropic glutamate receptors.
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Ayus, Juan Carlos, Steven G. Achinger, and Allen Arieff. "Brain cell volume regulation in hyponatremia: role of sex, age, vasopressin, and hypoxia." American Journal of Physiology-Renal Physiology 295, no. 3 (September 2008): F619—F624. http://dx.doi.org/10.1152/ajprenal.00502.2007.
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Hyponatremia is the most common electrolyte abnormality in hospitalized patients. When symptomatic (hyponatremic encephalopathy), the overall morbidity is 34%. Individuals most susceptible to death or permanent brain damage are prepubescent children and menstruant women. Failure of the brain to adapt to the hyponatremia leads to brain damage. Major factors that can impair brain adaptation include hypoxia and peptide hormones. In children, physical factors—discrepancy between skull size and brain size—are important in the genesis of brain damage. In adults, certain hormones—estrogen and vasopressin (usually elevated in cases of hyponatremia)—have been shown to impair brain adaptation, decreasing both cerebral blood flow and oxygen utilization. Initially, hyponatremia leads to an influx of water into the brain, primarily through glial cells and largely via the water channel aquaporin (AQP)4. Water is thus shunted into astrocytes, which swell, largely preserving neuronal cell volume. The initial brain response to swelling is adaptation, utilizing the Na+-K+-ATPase system to extrude cellular Na+. In menstruant women, estrogen + vasopressin inhibits the Na+-K+-ATPase system and decreases cerebral oxygen utilization, impairing brain adaptation. Cerebral edema compresses the respiratory centers and also forces blood out of the brain, both lowering arterial Po2 and decreasing oxygen utilization. The hypoxemia further impairs brain adaptation. Hyponatremic encephalopathy leads to brain damage when brain adaptation is impaired and is a consequence of both cerebral hypoxia and peptide hormones.
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GOODYEAR, MELINDA J., SHEILA G. CREWTHER, and BARBARA M. JUNGHANS. "A role for aquaporin-4 in fluid regulation in the inner retina." Visual Neuroscience 26, no. 2 (March 2009): 159–65. http://dx.doi.org/10.1017/s0952523809090038.
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AbstractMany diverse retinal disorders are characterized by retinal edema; yet, little experimental attention has been given to understanding the fundamental mechanisms underlying and contributing to these fluid-based disorders. Water transport in and out of cells is achieved by specialized membrane channels, with most rapid water transport regulated by transmembrane water channels known as aquaporins (AQPs). The predominant AQP in the mammalian retina is AQP4, which is expressed on the Müller glial cells. Müller cells have previously been shown to modulate neuronal activity by modifying the concentrations of ions, neurotransmitters, and other neuroactive substances within the extracellular space between the inner and the outer limiting membrane. In doing so, Müller cells maintain extracellular homeostasis, especially with regard to the spatial buffering of extracellular potassium (K+) via inward rectifying K+ channels (Kir channels). Recent studies of water transport and the spatial buffering of K+ through glial cells have highlighted the involvement of both AQP4 and Kir channels in regulating the extracellular environment in the brain and retina. As both glial functions are associated with neuronal activation, controversy exists in the literature as to whether the relationship is functionally dependent. It is argued in this review that as AQP4 channels are likely to be the conduit for facilitating fluid homeostasis in the inner retina during light activation, AQP4 channels are also likely to play a consequent role in the regulation of ocular volume and growth. Recent research has already shown that the level of AQP4 expression is associated with environmentally driven manipulations of light activity on the retina and the development of myopia.
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White, H. Steve, Sien Yao Chow, Y. C. Yen-Chow, and Dixon M. Woodbury. "Effect of elevated potassium on the ion content of mouse astrocytes and neurons." Canadian Journal of Physiology and Pharmacology 70, S1 (May 15, 1992): S263—S268. http://dx.doi.org/10.1139/y92-271.
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Potassium is tightly regulated within the extracellular compartment of the brain. Nonetheless, it can increase 3- to 4-fold during periods of intense seizure activity and 10- to 20-fold under certain pathological conditions such as spreading depression. Within the central nervous system, neurons and astrocytes are both affected by shifts in the extracellular concentration of potassium. Elevated potassium can lead to a redistribution of other ions (e.g., calcium, sodium, chloride, hydrogen, etc.) within the cellular compartment of the brain. Small shifts in the extracellular potassium concentration can markedly affect acid–base homeostasis, energy metabolism, and volume regulation of these two brain cells. Since normal neuronal function is tightly coupled to the ability of the surrounding glial cells to regulate ionic shifts within the brain and since both cell types can be affected by shifts in the extracellular potassium, it is important to characterize their individual response to an elevation of this ion. This review describes the results of side-by-side studies conducted on cortical neurons and astrocytes, which assessed the effect of elevated potassium on their resting membrane potential, intracellular volume, and their intracellular concentration of potassium, sodium, and chloride. The results obtained from these studies suggest that there exists a marked cellular heterogeneity between neurons and astrocytes in their response to an elevation in the extracellular potassium concentration.Key words: astrocytes, neurons, ion concentration, neuronal–glial interactions, mouse, cell culture.
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Potheraveedu, Veena Nambiar, Miriam Schöpel, Raphael Stoll, and Rolf Heumann. "Rheb in neuronal degeneration, regeneration, and connectivity." Biological Chemistry 398, no. 5-6 (May 1, 2017): 589–606. http://dx.doi.org/10.1515/hsz-2016-0312.
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AbstractThe small GTPase Rheb was originally detected as an immediate early response protein whose expression was induced by NMDA-dependent synaptic activity in the brain. Rheb’s activity is highly regulated by its GTPase activating protein (GAP), the tuberous sclerosis complex protein, which stimulates the conversion from the active, GTP-loaded into the inactive, GDP-loaded conformation. Rheb has been established as an evolutionarily conserved molecular switch protein regulating cellular growth, cell volume, cell cycle, autophagy, and amino acid uptake. The subcellular localization of Rheb and its interacting proteins critically regulate its activity and function. In stem cells, constitutive activation of Rheb enhances differentiation at the expense of self-renewal partially explaining the adverse effects of deregulated Rheb in the mammalian brain. In the context of various cellular stress conditions such as oxidative stress, ER-stress, death factor signaling, and cellular aging, Rheb activation surprisingly enhances rather than prevents cellular degeneration. This review addresses cell type- and cell state-specific function(s) of Rheb and mainly focuses on neurons and their surrounding glial cells. Mechanisms will be discussed in the context of therapy that interferes with Rheb’s activity using the antibiotic rapamycin or low molecular weight compounds.
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Alam, Sayed Ibrar, Min Gi Jo, Tae Ju Park, Rahat Ullah, Sareer Ahmad, Shafiq Ur Rehman, and Myeong Ok Kim. "Quinpirole-Mediated Regulation of Dopamine D2 Receptors Inhibits Glial Cell-Induced Neuroinflammation in Cortex and Striatum after Brain Injury." Biomedicines 9, no. 1 (January 7, 2021): 47. http://dx.doi.org/10.3390/biomedicines9010047.
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Brain injury is a significant risk factor for chronic gliosis and neurodegenerative diseases. Currently, no treatment is available for neuroinflammation caused by the action of glial cells following brain injury. In this study, we investigated the quinpirole-mediated activation of dopamine D2 receptors (D2R) in a mouse model of traumatic brain injury (TBI). We also investigated the neuroprotective effects of quinpirole (a D2R agonist) against glial cell-induced neuroinflammation secondary to TBI in adult mice. After the brain injury, we injected quinpirole into the TBI mice at a dose of 1 mg/kg daily intraperitoneally for 7 days. Our results showed suppression of D2R expression and deregulation of downstream signaling molecules in ipsilateral cortex and striatum after TBI on day 7. Quinpirole administration regulated D2R expression and significantly reduced glial cell-induced neuroinflammation via the D2R/Akt/glycogen synthase kinase 3 beta (GSK3-β) signaling pathway after TBI. Quinpirole treatment concomitantly attenuated increase in glial cells, neuronal apoptosis, synaptic dysfunction, and regulated proteins associated with the blood–brain barrier, together with the recovery of lesion volume in the TBI mouse model. Additionally, our in vitro results confirmed that quinpirole reversed the microglial condition media complex-mediated deleterious effects and regulated D2R levels in HT22 cells. This study showed that quinpirole administration after TBI reduced secondary brain injury-induced glial cell activation and neuroinflammation via regulation of the D2R/Akt/GSK3-β signaling pathways. Our study suggests that quinpirole may be a safe therapeutic agent against TBI-induced neurodegeneration.
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Song, Daisheng, Keith A. Sharkey, Deanne R. Breitman, Yikun Zhang, and Samuel S. Lee. "Disordered central cardiovascular regulation in portal hypertensive and cirrhotic rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 280, no. 3 (March 1, 2001): G420—G430. http://dx.doi.org/10.1152/ajpgi.2001.280.3.g420.
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Portal hypertension due to either prehepatic portal hypertension or cirrhosis is associated with cardiovascular derangement. We aimed to delineate regulatory mechanisms in the brain stem cardiovascular nuclei in rat models of prehepatic portal hypertension and cirrhosis. Neuronal activation in the nucleus of the solitary tract (NTS) and ventrolateral medulla (VLM) were assessed by immunohistochemical staining for the immediate-early gene product Fos. In the same sections, catecholaminergic neurons were counted by tyrosine hydroxylase (TH) staining. Ninety minutes after hypotensive hemorrhage (or no volume challenge), the animals were killed for Fos and TH medullary staining. These protocols were repeated after capsaicin administration. The NTS of unchallenged sham-operated rats had scant Fos-positive cells (3.6 ± 0.4 cells/section), whereas hemorrhage significantly increased Fos staining (91.8 ± 14). In contrast, the unchallenged portal hypertensive and cirrhotic groups showed increased Fos staining (14.3 ± 5.8 and 32.8 ± 2.8, respectively), which hemorrhage did not alter significantly. The numbers of TH-positive cells were similar in the three unchallenged groups; double labeling revealed that ∼50% of TH-positive cells were activated by hemorrhage in the sham and cirrhotic rats but not the portal hypertensive rats. Similar patterns of Fos and TH staining were observed in the VLM. Capsaicin treatment not only significantly reduced the Fos-positive neuron numbers in portal hypertensive and cirrhotic rats but also attenuated hemorrhage-induced Fos and double-positive cells in both NTS and VLM. These results suggest that disordered trafficking in capsaicin-sensitive nerves and central dysregulation contribute to blunted cardiovascular responsiveness in cirrhosis and prehepatic portal hypertension.
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Altmann, Patrick, Michael Mildner, Thomas Haider, Denise Traxler, Lucian Beer, Robin Ristl, Bahar Golabi, Christian Gabriel, Fritz Leutmezer, and Hendrik Jan Ankersmit. "Secretomes of apoptotic mononuclear cells ameliorate neurological damage in rats with focal ischemia." F1000Research 3 (October 28, 2014): 131. http://dx.doi.org/10.12688/f1000research.4219.2.
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The pursuit of targeting multiple pathways in the ischemic cascade of cerebral stroke is a promising treatment option. We examined the regenerative potential of conditioned medium derived from rat and human apoptotic mononuclear cells (MNC), rMNCapo sec and hMNCapo sec, in experimental stroke.We performed middle cerebral artery occlusion on Wistar rats and administered apoptotic MNC-secretomes intraperitoneally in two experimental settings. Ischemic lesion volumes were determined 48 hours after cerebral ischemia. Neurological evaluations were performed after 6, 24 and 48 hours. Immunoblots were conducted to analyze neuroprotective signal-transduction in human primary glia cells and neurons. Neuronal sprouting assays were performed and neurotrophic factors in both hMNCapo sec and rat plasma were quantified using ELISA.Administration of rat as well as human apoptotic MNC-secretomes significantly reduced ischemic lesion volumes by 36% and 37%, respectively. Neurological examinations revealed improvement after stroke in both treatment groups. Co-incubation of human astrocytes, Schwann cells and neurons with hMNCapo sec resulted in activation of several signaling cascades associated with the regulation of cytoprotective gene products and enhanced neuronal sprouting in vitro. Analysis of neurotrophic factors in hMNCapo sec and rat plasma revealed high levels of brain derived neurotrophic factor (BDNF).Our data indicate that apoptotic MNC-secretomes elicit neuroprotective effects on rats that have undergone ischemic stroke.
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Walch, Erin, Thomas R. Murphy, Nicholas Cuvelier, Murad Aldoghmi, Cristine Morozova, Jordan Donohue, Gaby Young, et al. "Astrocyte-Selective Volume Increase in Elevated Extracellular Potassium Conditions Is Mediated by the Na+/K+ ATPase and Occurs Independently of Aquaporin 4." ASN Neuro 12 (January 2020): 175909142096715. http://dx.doi.org/10.1177/1759091420967152.
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Astrocytes and neurons have been shown to swell across a variety of different conditions, including increases in extracellular potassium concentration (^[K+]o). The mechanisms involved in the coupling of K+ influx to water movement into cells leading to cell swelling are not well understood and remain controversial. Here, we set out to determine the effects of ^[K+]o on rapid volume responses of hippocampal CA1 pyramidal neurons and stratum radiatum astrocytes using real-time confocal volume imaging. First, we found that elevating [K+]o within a physiological range (to 6.5 mM and 10.5 mM from a baseline of 2.5 mM), and even up to pathological levels (26 mM), produced dose-dependent increases in astrocyte volume, with absolutely no effect on neuronal volume. In the absence of compensating for addition of KCl by removal of an equal amount of NaCl, neurons actually shrank in ^[K+]o, while astrocytes continued to exhibit rapid volume increases. Astrocyte swelling in ^[K+]o was not dependent on neuronal firing, aquaporin 4, the inwardly rectifying potassium channel Kir 4.1, the sodium bicarbonate cotransporter NBCe1, , or the electroneutral cotransporter, sodium-potassium-chloride cotransporter type 1 (NKCC1), but was significantly attenuated in 1 mM barium chloride (BaCl2) and by the Na+/K+ ATPase inhibitor ouabain. Effects of 1 mM BaCl2 and ouabain applied together were not additive and, together with reports that BaCl2 can inhibit the NKA at high concentrations, suggests a prominent role for the astrocyte NKA in rapid astrocyte volume increases occurring in ^[K+]o. These findings carry important implications for understanding mechanisms of cellular edema, regulation of the brain extracellular space, and brain tissue excitability.
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Shi, Hong, Baiyang Sheng, Feng Zhang, Chunying Wu, Rongli Zhang, Junqing Zhu, Kui Xu, et al. "Kruppel-like factor 2 protects against ischemic stroke by regulating endothelial blood brain barrier function." American Journal of Physiology-Heart and Circulatory Physiology 304, no. 6 (March 15, 2013): H796—H805. http://dx.doi.org/10.1152/ajpheart.00712.2012.
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During an ischemic stroke normal brain endothelial function is perturbed, resulting in blood brain barrier (BBB) breakdown with subsequent infiltration of activated inflammatory blood cells, ultimately leading to neuronal cell death. Kruppel-like factor 2 (KLF2) is regulated by flow, is highly expressed in vascular endothelial cells (ECs), and serves as a key molecular switch regulating endothelial function and promoting vascular health. In this study we sought to determine the role of KLF2 in cerebrovascular function and the pathogenesis of ischemic stroke. Transient middle cerebral artery occlusion was performed in KLF2-deficient (KLF2−/−), KLF2 overexpressing (KLF2tg), and control mice, and stroke volume was analyzed. BBB function was assessed in vivo by real-time neuroimaging using positron emission tomography and Evan's blue dye assay. KLF2−/− mice exhibited significantly larger strokes and impairment in BBB function. In contrast, KLF2tg mice were protected against ischemic stroke and demonstrated preserved BBB function. In concordance, gain- and loss-of-function studies in primary brain microvascular ECs using transwell assays revealed KLF2 to be BBB protective. Mechanistically, KLF2 was demonstrated, both in vitro and in vivo, to regulate the critical BBB tight junction factor occludin. These data are first to identify endothelial KLF2 as a key regulator of the BBB and a novel neuroprotective factor in ischemic stroke.
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Jiang, Yuanding, Tao Wang, Jian He, Quan Liao, and Jingjing Wang. "Influence of miR-1 on Nerve Cell Apoptosis in Rats with Cerebral Stroke via Regulating ERK Signaling Pathway." BioMed Research International 2021 (August 19, 2021): 1–8. http://dx.doi.org/10.1155/2021/9988534.
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To explore the effect of miR-1 on neuronal apoptosis in rats with stroke through the ERK signaling pathway. Methods. Forty male rats (180-220 g) were selected and randomly divided into the sham, model, miR-1 inhibitor, and miR-1 mimic groups (10 rats per group) by average body weight. Cerebral ischemia/reperfusion (I/R) models were established using a modified middle cerebral artery wire thrombosis (MCAO) method in rats in the model group, miR-1 inhibitor group, and miR-1 mimic group. After the successful model establishment, the miR-1inhibitor group and miR-1 mimic group were intravenously injected with miR-1 inhibitor and miR-1 mimic, respectively, once a day for 3 days. The sham and model groups were given the same dose of normal saline. TTC staining was applied to detect the cerebral infarct size and calculate the infarct volume. Histopathological changes in the hippocampus of rat brains were observed by HE staining. Flow cytometry was used to detect neuronal apoptosis in rat brains. The mRNA expressions of miR-1, ERK1/2, Bcl-2, and Bax in rat brain tissues were determined by QRT PCR, and the protein levels of ERK1/2, Bcl-2, Bax, and caspase-3 were determined by Western blot analysis. Results. Compared with the sham group, the neurological impairment score, cerebral infarct size, and volume of rats in the model group were significantly increased ( p < 0.05 ). Compared with the model group, the neurological impairment score, cerebral infarct size, and volume were significantly increased in the miR-1 mimic group and significantly decreased in the miR-1 inhibitor group ( p < 0.05 ). In the model group, the hippocampal tissue of rats had malaligned cells, neuron cell atrophy became smaller, the intercellular spaces became larger, and vacuoles appeared. Compared with the model group, the miR-1 inhibitor group could effectively alleviate the pathological changes in the hippocampus, and the miR-1 mimic group could significantly add to the pathological changes in the rat hippocampus. Compared with the sham group, the mRNA expression of miR-1 and Bax in the brain of model rats increased significantly ( p < 0.05 ), and the mRNA expression of ERK1/2 decreased significantly; Compared with the model group, the miR-1 and Bax mRNA expressions in the brain tissues of rats in the miR-1 inhibitor group were significantly decreased, the ERK1/2 and bcl-2 mRNA expressions were significantly increased, and the miR-1 and Bax mRNA expressions in the brain tissues of rats in the miR-1 inhibitor group were significantly decreased, and the Bcl-2 mRNA expression was significantly increased ( p < 0.05 ). Compared with the sham group, neuronal apoptosis was increased in the brain tissues of rats in the model group and miR-1 mimic group. Compared with the model group, neuronal apoptosis was decreased in the brain tissues of rats in the miR-1 inhibitor group. Compared with the sham group, the ERK1/2 proteins in the model group were significantly decreased, the Bcl-2, Bax, and caspase-3 proteins were significantly increased, and the ERK1/2, Bcl-2, Bax, and caspase-3 proteins in the miR-1 inhibitor group and miR-1 mimic group were significantly increased. Compared with the model group, the protein levels of ERK1/2 and Bcl-2 in the miR-1 inhibitor group were significantly increased, the proteins of Bax and caspase-3 were significantly decreased, and the protein levels of ERK1/2 and Bcl-2 in the miR-1 inhibitor group were significantly increased ( p < 0.05 ). Conclusions. miR-1 can interfere with neuronal apoptosis in rats with stroke through the ERK signaling pathway.
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Wan, Jing-zhi, Rui Wang, Zhi-yong Zhou, Li-li Deng, Chang-cheng Zhang, Chao-qi Liu, Hai-xia Zhao, et al. "Saponins of Panax japonicus Confer Neuroprotection against Brain Aging through Mitochondrial Related Oxidative Stress and Autophagy in Rats." Current Pharmaceutical Biotechnology 21, no. 8 (July 8, 2020): 667–80. http://dx.doi.org/10.2174/1389201021666191216114815.
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Background: Oxidative stress and mitochondrial dysfunction play a vital role in the pathogenesis of brain aging. Saponins from Panax japonicus (SPJ) have attracted much attention for their potential to attenuate age-related oxidative stress as the main ingredient in rhizomes of Panax japonicus. Objective: This study aimed to investigate the neuroprotective effects of SPJ on natural aging rats as well as the underlying mechanisms regarding oxidative stress and mitochondrial pathway. Methods: Sprague-Dawley rats were divided into control groups (3-, 9-, 15- and 24-month old groups) and SPJ-treated groups. For SPJ-treated groups, SPJ were orally administrated to 18-month old rats at doses of 10 mg/kg, 30 mg/kg and 60 mg/kg once daily. Control groups were given the same volume of saline. After the treatment with SPJ or saline for six months, the cortex and hippocampus were rapidly harvested and deposited at -80°C after the rats were decapitated under anesthesia. The neuroprotective effects of SPJ were estimated by histopathological observation, TUNEL detection, biochemical determination and western blotting. Results: SPJ improved pathomorphological changes in neuronal cells and decreased apoptosis in the cortex and hippocampus of aging rats, increased the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), Na+/K+-ATPase, Ca2+-ATPase and Ca2+/Mg2+-ATPase whereas, decreased malondialdehyde (MDA) contents in the cortex of aging rats. Furthermore, the SPJ increased silent mating type information regulation 2 homolog-1 (SIRT1) protein expression, decreased acetylated level of peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) in the cortex and hippocampus of aging rats, and reversed the aging-induced decline of Forkhead box O3 (Foxo3a), Superoxide Dismutase 2 (SOD2), microtubule-associated protein light chain 3 (LC3II) and Beclin1 levels in the cortex and hippocampus. Conclusion: Our data showed that SPJ conferred neuroprotection partly through the regulation of oxidative stress and mitochondria-related pathways in aging rats.
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Hys, Michał, Nikodem Skoczeń, Ewelina Soroka, and Marcin Olajossy. "Structural and functional changes in the central nervous system in the course of anorexia nervosa." Current Problems of Psychiatry 18, no. 4 (December 1, 2017): 321–30. http://dx.doi.org/10.1515/cpp-2017-0025.
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AbstractNew achievements within structural and functional imaging of central nervous system offer a basis for better understanding of the mechanisms underlying many mental disorders. In everyday clinical practice, we encounter many difficulties in the therapy of eating disorders. They are caused by a complex psychopathological picture, varied grounds of the problems experienced by patients, often poor motivation for active participation in the treatment process, difficulties in communication between patients and therapeutic staff, and various biological conditions of eating disorders. In this paper, the latest reports on new concepts and methods of diagnosis and treatment of anorexia nervosa have been analyzed. The selection of the analyzed publications was based on the criteria taking into account the time of publication, the size of research cohorts, as well as the experience of research teams in the field of nutritional disorders, confirmed by the number of works and their citations. The work aims to spread current information on anorexia nervosa neurobiology that would allow for determining the brain regions involved in the regulation of food intake, and consequently that may be a potential place where neurobiochemical processes responsible for eating disorders occur. In addition, using modern methods of structural imaging, the authors want to show some of the morphometric variations, particularly within white matter, occurring in patients suffering from anorexia nervosa, as well as those evaluated with magnetoencephalography of processes associated with the neuronal processing of information related to food intake. For example as regards anorexia nervosa, it was possible to localize the areas associated with eating disorders and broaden our knowledge about the changes in these areas that cause and accompany the illness. The described in this paper research studies using diffusion MRI fiber tractography showed the presence of changes in the white matter pathways of the brain, especially in the corpus callosum, which indicate a reduced content of myelin. These changes probably reflect malnutrition, and directly represent the effect of lipid deficiency. This leads to a weakening of the structure, and even cell death. In addition, there are more and more reports that show the normal volume of brain cells in patients with long-term remission of anorexia. It was also shown that in patients in remission stage there are functional changes within the amygdala in response to a task not related symptomatologically with anorexia nervosa. The appearing in the scientific literature data stating that in patients with anorexia nervosa there is a reduced density of GFAP + cells of the hippocampus and increased expression of vimentin and nestin, is also worth noting.
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Kukucka, Jessica, Tessa Wyllie, Justin Read, Lauren Mahoney, and Cenk Suphioglu. "Human neuronal cells: epigenetic aspects." BioMolecular Concepts 4, no. 4 (August 1, 2013): 319–33. http://dx.doi.org/10.1515/bmc-2012-0053.
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AbstractHistone acetyltransferases (HATs) and histone deacetylases (HDACs) promote histone posttranslational modifications, which lead to an epigenetic alteration in gene expression. Aberrant regulation of HATs and HDACs in neuronal cells results in pathological consequences such as neurodegeneration. Alzheimer’s disease is the most common neurodegenerative disease of the brain, which has devastating effects on patients and loved ones. The use of pan-HDAC inhibitors has shown great therapeutic promise in ameliorating neurodegenerative ailments. Recent evidence has emerged suggesting that certain deacetylases mediate neurotoxicity, whereas others provide neuroprotection. Therefore, the inhibition of certain isoforms to alleviate neurodegenerative manifestations has now become the focus of studies. In this review, we aimed to discuss and summarize some of the most recent and promising findings of HAT and HDAC functions in neurodegenerative diseases.
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Pasantes-Morales, H. "Volume regulation in brain cells: Cellular and molecular mechanisms." Metabolic Brain Disease 11, no. 3 (September 1996): 187–204. http://dx.doi.org/10.1007/bf02237957.
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D'Asti, Esterina, Annie Huang, Marcel Kool, Brian Meehan, Jennifer A. Chan, Nada Jabado, Andrey Korshunov, Stefan M. Pfister, and Janusz Rak. "Tissue Factor Regulation by miR-520g in Primitive Neuronal Brain Tumor Cells." American Journal of Pathology 186, no. 2 (February 2016): 446–59. http://dx.doi.org/10.1016/j.ajpath.2015.10.020.
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McManus, M. L., and K. Strange. "RAPID VOLUME REGULATION IN BRAIN CELLS EXPOSED TO HYPERTONIC SALINE." Journal of Neurosurgical Anesthesiology 4, no. 4 (October 1992): 300. http://dx.doi.org/10.1097/00008506-199210000-00020.
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McManus, Michael L., and Kevin Strange. "Acute Volume Regulation of Brain Cells in Response to Hypertonic Challenge." Anesthesiology 78, no. 6 (June 1, 1993): 1132–37. http://dx.doi.org/10.1097/00000542-199306000-00017.
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Strange, K., and R. Morrison. "Volume regulation during recovery from chronic hypertonicity in brain glial cells." American Journal of Physiology-Cell Physiology 263, no. 2 (August 1, 1992): C412—C419. http://dx.doi.org/10.1152/ajpcell.1992.263.2.c412.
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Rat C6 glial cells undergo rapid regulatory volume increase (5-10 min) via electrolyte uptake when exposed to a hypertonic medium. With chronic exposure to hypertonicity (greater than 8 h), accumulated electrolyte is replaced partly by inositol. Inositol accumulation is brought about by upregulation of Na(+)-dependent inositol transport. When C6 cells acclimated chronically to hypertonic NaCl medium were returned to isotonic conditions, inositol levels dropped slowly from 478 nmol/mg protein towards control values (117 nmol/mg protein) in 18-24 h. Inositol loss occurred in part by efflux to the external medium via a pathway distinct from the uptake mechanism. Laser light-scattering measurements demonstrated that regulatory volume decrease (RVD) is slow under these experimental conditions. In contrast, cells exposed acutely to hypertonicity swell and then undergo a rapid and nearly complete RVD when returned to isotonic medium. These results suggest that slow inositol loss is rate limiting for RVD during recovery from chronic hypertonic stress. The slow inositol loss and RVD may be due to slow turnover of the efflux mechanism and/or slow downregulation of the hypertonically stimulated inositol uptake pathway.
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Zhao, Xiang, Ari Rouhiainen, Zhilin Li, Su Guo, and Heikki Rauvala. "Regulation of Neurogenesis in Mouse Brain by HMGB1." Cells 9, no. 7 (July 17, 2020): 1714. http://dx.doi.org/10.3390/cells9071714.
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The High Mobility Group Box 1 (HMGB1) is the most abundant nuclear nonhistone protein that is involved in transcription regulation. In addition, HMGB1 has previously been found as an extracellularly acting protein enhancing neurite outgrowth in cultured neurons. Although HMGB1 is widely expressed in the developing central nervous system of vertebrates and invertebrates, its function in the developing mouse brain is poorly understood. Here, we have analyzed developmental defects of the HMGB1 null mouse forebrain, and further examined our findings in ex vivo brain cell cultures. We find that HMGB1 is required for the proliferation and differentiation of neuronal stem cells/progenitor cells. Enhanced apoptosis is also found in the neuronal cells lacking HMGB1. Moreover, HMGB1 depletion disrupts Wnt/β-catenin signaling and the expression of transcription factors in the developing cortex, including Foxg1, Tbr2, Emx2, and Lhx6. Finally, HMGB1 null mice display aberrant expression of CXCL12/CXCR4 and reduced RAGE signaling. In conclusion, HMGB1 plays a critical role in mammalian neurogenesis and brain development.
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Ortega, Sterling B., Vanessa O. Torres, Sarah E. Latchney, Cody W. Whoolery, Ibrahim Z. Noorbhai, Katie Poinsatte, Uma M. Selvaraj, et al. "B cells migrate into remote brain areas and support neurogenesis and functional recovery after focal stroke in mice." Proceedings of the National Academy of Sciences 117, no. 9 (February 12, 2020): 4983–93. http://dx.doi.org/10.1073/pnas.1913292117.
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Lymphocytes infiltrate the stroke core and penumbra and often exacerbate cellular injury. B cells, however, are lymphocytes that do not contribute to acute pathology but can support recovery. B cell adoptive transfer to mice reduced infarct volumes 3 and 7 d after transient middle cerebral artery occlusion (tMCAo), independent of changing immune populations in recipient mice. Testing a direct neurotrophic effect, B cells cocultured with mixed cortical cells protected neurons and maintained dendritic arborization after oxygen-glucose deprivation. Whole-brain volumetric serial two-photon tomography (STPT) and a custom-developed image analysis pipeline visualized and quantified poststroke B cell diapedesis throughout the brain, including remote areas supporting functional recovery. Stroke induced significant bilateral B cell diapedesis into remote brain regions regulating motor and cognitive functions and neurogenesis (e.g., dentate gyrus, hypothalamus, olfactory areas, cerebellum) in the whole-brain datasets. To confirm a mechanistic role for B cells in functional recovery, rituximab was given to human CD20+(hCD20+) transgenic mice to continuously deplete hCD20+-expressing B cells following tMCAo. These mice experienced delayed motor recovery, impaired spatial memory, and increased anxiety through 8 wk poststroke compared to wild type (WT) littermates also receiving rituximab. B cell depletion reduced stroke-induced hippocampal neurogenesis and cell survival. Thus, B cell diapedesis occurred in areas remote to the infarct that mediated motor and cognitive recovery. Understanding the role of B cells in neuronal health and disease-based plasticity is critical for developing effective immune-based therapies for protection against diseases that involve recruitment of peripheral immune cells into the injured brain.
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Matsubara, Shuzo, Taito Matsuda, and Kinichi Nakashima. "Regulation of Adult Mammalian Neural Stem Cells and Neurogenesis by Cell Extrinsic and Intrinsic Factors." Cells 10, no. 5 (May 10, 2021): 1145. http://dx.doi.org/10.3390/cells10051145.
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Tissue-specific stem cells give rise to new functional cells to maintain tissue homeostasis and restore damaged tissue after injury. To ensure proper brain functions in the adult brain, neural stem cells (NSCs) continuously generate newborn neurons that integrate into pre-existing neuronal networks. Proliferation, as well as neurogenesis of NSCs, are exquisitely controlled by extrinsic and intrinsic factors, and their underlying mechanisms have been extensively studied with the goal of enhancing the neurogenic capacity of NSCs for regenerative medicine. However, neurogenesis of endogenous NSCs alone is insufficient to completely repair brains damaged by neurodegenerative diseases and/or injury because neurogenic areas are limited and few neurons are produced in the adult brain. An innovative approach towards replacing damaged neurons is to induce conversion of non-neuronal cells residing in injured sites into neurons by a process referred to as direct reprogramming. This review describes extrinsic and intrinsic factors controlling NSCs and neurogenesis in the adult brain and discusses prospects for their applications. It also describes direct neuronal reprogramming technology holding promise for future clinical applications.
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Hamano, Hiroko, Masashi Noguchi, Hidekimi Fukui, Atsushi Issiki, and Yasuo Watanabe. "Regulation of brain cell environment on neuronal protection: role of TNFα in glia cells." Life Sciences 72, no. 4-5 (December 2002): 565–74. http://dx.doi.org/10.1016/s0024-3205(02)02252-x.
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Andrew, R. David, Michael E. Lobinowich, and E. Philip Osehobo. "Evidence against Volume Regulation by Cortical Brain Cells during Acute Osmotic Stress." Experimental Neurology 143, no. 2 (February 1997): 300–312. http://dx.doi.org/10.1006/exnr.1996.6375.
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Kareva, E. N., О. M. Oleynikova, V. O. Panov, N. L. Shimanovskiy, and V. I. Skvortsova. "ESTROGENS AND BRAIN." Annals of the Russian academy of medical sciences 67, no. 2 (February 22, 2012): 48–59. http://dx.doi.org/10.15690/vramn.v67i2.122.
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Recent data upon molecular mechanisms of pleiotropic action of estrogens in human brain is presented in the article. Given detailed descriptions of properties of classical and membrane bound estradiol receptors, that maintain gene expression regulation, modulation of neurotransmittent systems and signal cascade activation in neuronal cells. Data upon regional distribution of estradiol receptor subtypes in the brain, their participation in main cell population function control (including progenitor cells) is given. Special attention is paid to estrogen participation in neurogenesis, inflammation and apoptosis regulation in central nervous system; in the control of formation and functioning of cerebral vessels.
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Munier, Mathilde, Geri Meduri, Say Viengchareun, Philippe Leclerc, Damien Le Menuet, and Marc Lombès. "Regulation of Mineralocorticoid Receptor Expression during Neuronal Differentiation of Murine Embryonic Stem Cells." Endocrinology 151, no. 5 (March 5, 2010): 2244–54. http://dx.doi.org/10.1210/en.2009-0753.
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Mineralocorticoid receptor (MR) plays a critical role in brain function. However, the regulatory mechanisms controlling neuronal MR expression that constitutes a key element of the hormonal response are currently unknown. Two alternative P1 and P2 promoters drive human MR gene transcription. To examine promoter activities and their regulation during neuronal differentiation and in mature neurons, we generated stably transfected recombinant murine embryonic stem cell (ES) lines, namely P1-GFP and P2-GFP, in which each promoter drove the expression of the reporter gene green fluorescent protein (GFP). An optimized protocol, using embryoid bodies and retinoic acid, permitted us to obtain a reproducible neuronal differentiation as revealed by the decrease in phosphatase alkaline activity, the concomitant appearance of morphological changes (neurites), and the increase in the expression of neuronal markers (nestin, β-tubulin III, and microtubule-associated protein-2) as demonstrated by immunocytochemistry and quantitative PCR. Using these cell-based models, we showed that MR expression increased by 5-fold during neuronal differentiation, MR being preferentially if not exclusively expressed in mature neurons. Although the P2 promoter was always weaker than the P1 promoter during neuronal differentiation, their activities increased by 7- and 5-fold, respectively, and correlated with MR expression. Finally, although progesterone and dexamethasone were ineffective, aldosterone stimulated both P1 and P2 activity and MR expression, an effect that was abrogated by knockdown of MR by small interfering RNA. In conclusion, we provide evidence for a tight transcriptional control of MR expression during neuronal differentiation. Given the neuroprotective and antiapoptotic role proposed for MR, the neuronal differentiation of ES cell lines opens potential therapeutic perspectives in neurological and psychiatric diseases.
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Salmina, A. B., A. I. Inzhutova, A. V. Morgun, O. S. Okuneva, N. A. Malinovskaya, O. L. Lopatina, M. M. Petrova, T. E. Taranunushenko, A. A. Fursov, and N. V. Kuvacheva. "NAD+-CONVERTING ENZYMES IN NEURONAL AND GLIAL CELLS: CD38 AS A NOVEL TARGET FOR NEUROPROTECTION." Annals of the Russian academy of medical sciences 67, no. 10 (October 10, 2012): 29–37. http://dx.doi.org/10.15690/vramn.v67i10.413.
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The review contains current data on molecular mechanisms which control NAD+ homeostasis in brain cells. It also deals with the role of NAD+-converting enzymes in regulation of functional activity, viability and intercellular communication of neuronal and glial cells. Special attention is paid to involvement of CD38 into regulation of NAD+ levels in brain cells in normal and pathological conditions.
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Selmaj, Krzysztof, Zofia Pawłowska, Agata Walczak, Wiktor Koziołkiewicz, Cedric S. Raine, and Czesław S. Cierniewski. "Corpora amylacea from multiple sclerosis brain tissue consists of aggregated neuronal cells." Acta Biochimica Polonica 55, no. 1 (February 5, 2008): 43–50. http://dx.doi.org/10.18388/abp.2008_3199.
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In this report, we describe proteomic analysis of corpora amylacea collected by postmortem laser microdissection from multiple sclerosis (MS) brain lesions. Using low level protein loads (about 30 microg), a combination of two-dimensional electrophoresis with matrix-assisted laser desorption/ionization-time of flight mass spectrometry and database interrogations we identified 24 proteins of suspected neuronal origin. In addition to major cytoskeletal proteins like actin, tubulin, and vimentin, we identified a variety of proteins implicated specifically in cellular motility and plasticity (F-actin capping protein), regulation of apoptosis and senescence (tumor rejection antigen-1, heat shock proteins, valosin-containing protein, and ubiquitin-activating enzyme E1), and enzymatic pathways (glyceraldehyde-3-dehydrogenase, protein disulfide isomerase, protein disulfide isomerase related protein 5, lactate dehydrogenase). Samples taken from regions in the vicinity of corpora amylacea showed only traces of cellular proteins suggesting that these bodies may represent remnants of neuronal aggregates with highly polymerized cytoskeletal material. Our data provide evidence supporting the concept that biogenesis of corpora amylacea involves degeneration and aggregation of cells of neuronal origin.
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Wang, Chaoyun, Hongzhi Wan, Qiaoyun Wang, Hongliu Sun, Yeying Sun, Kexin Wang, and Chunxiang Zhang. "Safflor Yellow B Attenuates Ischemic Brain Injury via Downregulation of Long Noncoding AK046177 and Inhibition of MicroRNA-134 Expression in Rats." Oxidative Medicine and Cellular Longevity 2020 (June 4, 2020): 1–20. http://dx.doi.org/10.1155/2020/4586839.
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Stroke breaks the oxidative balance in the body and causes extra reactive oxygen species (ROS) generation, leading to oxidative stress damage. Long noncoding RNAs (lncRNAs) and microRNAs play pivotal roles in oxidative stress-mediated brain injury. Safflor yellow B (SYB) was able to effectively reduce ischemia-mediated brain damage by increasing antioxidant capacity and inhibiting cell apoptosis. In this study, we investigated the putative involvement of lncRNA AK046177 and microRNA-134 (miR-134) regulation in SYB against ischemia/reperfusion- (I/R-) induced neuronal injury. I/R and oxygen-glucose deprivation/reoxygenation (OGD/R) were established in vivo and in vitro. Cerebral infarct volume, neuronal apoptosis, and protein expression were detected. The effects of SYB on cell activity, cell respiration, nuclear factor erythroid 2-related factor 2 (Nrf2), antioxidant enzymes, and ROS were evaluated. I/R or OGD/R upregulated the expression of AK046177 and miR-134 and subsequently inhibited the activation and expression of CREB, which caused ROS generation and brain/cell injury. SYB attenuated the effects of AK046177, inhibited miR-134 expression, and promoted CREB activation, which in turn promoted Nrf2 expression, and then increased antioxidant capacities, improved cell respiration, and reduced apoptosis. We suggested that the antioxidant effects of SYB were driven by an AK046177/miR-134/CREB-dependent mechanism that inhibited this pathway, and that SYB has potential use in reducing or possibly preventing I/R-induced neuronal injury.
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Urbainsky, Claudia, Rolf Nölker, Marcel Imber, Adrian Lübken, Jörg Mostertz, Falko Hochgräfe, José R. Godoy, Eva-Maria Hanschmann, and Christopher Horst Lillig. "Nucleoredoxin-Dependent Targets and Processes in Neuronal Cells." Oxidative Medicine and Cellular Longevity 2018 (November 21, 2018): 1–11. http://dx.doi.org/10.1155/2018/4829872.
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Nucleoredoxin (Nrx) is an oxidoreductase of the thioredoxin family of proteins. It was shown to act as a signal transducer in some pathways; however, so far, no comprehensive analysis of its regulated substrates and functions was available. Here, we used a combination of two different strategies to fill this gap. First, we analyzed the thiol-redox state of the proteome of SH-SY5Y neuroblastoma cells depleted of Nrx compared to control cells using a differential thiol-labeling technique and quantitative mass spectrometry. 171 proteins were identified with an altered redox state; 161 of these were more reduced in the absence of Nrx. This suggests functions of Nrx in the oxidation of protein thiols. Second, we utilized the active site mutant Cys208Ser of Nrx, which stabilizes a mixed disulfide intermediate with its substrates and therefore trapped interacting proteins from the mouse brain (identifying 1710 proteins) and neuronal cell culture extracts (identifying 609 proteins). Profiling of the affected biological processes and molecular functions in cells of neuronal origin suggests numerous functions of Nrx in the redox regulation of metabolic pathways, cellular morphology, and signal transduction. These results characterize Nrx as a cellular oxidase that itself may be oxidized by the formation of disulfide relays with peroxiredoxins.
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Pérez-Sen, Queipo, Gil-Redondo, Ortega, Gómez-Villafuertes, Miras-Portugal, and Delicado. "Dual-Specificity Phosphatase Regulation in Neurons and Glial Cells." International Journal of Molecular Sciences 20, no. 8 (April 23, 2019): 1999. http://dx.doi.org/10.3390/ijms20081999.
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Dual-specificity protein phosphatases comprise a protein phosphatase subfamily with selectivity towards mitogen-activated protein (MAP) kinases, also named MKPs, or mitogen-activated protein kinase (MAPK) phosphatases. As powerful regulators of the intensity and duration of MAPK signaling, a relevant role is envisioned for dual-specificity protein phosphatases (DUSPs) in the regulation of biological processes in the nervous system, such as differentiation, synaptic plasticity, and survival. Important neural mediators include nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) that contribute to DUSP transcriptional induction and post-translational mechanisms of DUSP protein stabilization to maintain neuronal survival and differentiation. Potent DUSP gene inducers also include cannabinoids, which preserve DUSP activity in inflammatory conditions. Additionally, nucleotides activating P2X7 and P2Y13 nucleotide receptors behave as novel players in the regulation of DUSP function. They increase cell survival in stressful conditions, regulating DUSP protein turnover and inducing DUSP gene expression. In general terms, in the context of neural cells exposed to damaging conditions, the recovery of DUSP activity is neuroprotective and counteracts pro-apoptotic over-activation of p38 and JNK. In addition, remarkable changes in DUSP function take place during the onset of neuropathologies. The restoration of proper DUSP levels and recovery of MAPK homeostasis underlie the therapeutic effect, indicating that DUSPs can be relevant targets for brain diseases.
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Brenneman, D. E., E. A. Neale, G. A. Foster, S. W. d'Autremont, and G. L. Westbrook. "Nonneuronal cells mediate neurotrophic action of vasoactive intestinal peptide." Journal of Cell Biology 104, no. 6 (June 1, 1987): 1603–10. http://dx.doi.org/10.1083/jcb.104.6.1603.
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The developmental regulation of neuronal survival by vasoactive intestinal peptide (VIP) was investigated in dissociated spinal cord-dorsal root ganglion (SC-DRG) cultures. Previous studies demonstrated that VIP increased neuronal survival in SC-DRG cultures when synaptic transmission was blocked with tetrodotoxin (TTX). This effect was further investigated to determine if VIP acted directly on neurons or via nonneuronal cells. For these studies, SC-DRG cells were cultured under conditions designed to provide preparations enriched for a particular cell type: astrocyte-enriched background cell (BG) cultures, meningeal fibroblast cultures, standard mixed neuron-nonneuron (STD) cultures, and neuron-enriched (N) cultures. Addition of 0.1 nM VIP to TTX-treated STD cultures for 5 d prevented the TTX-mediated death and the death that occurred naturally during development in culture, whereas the same treatment on N cultures did not prevent neuronal cell death. Conditioned medium from VIP-stimulated BG cultures prevented neuronal cell death when added to the medium (10% of total volume) of N cultures treated with TTX. The same amount of conditioned medium from BG cultures that were not treated with VIP had no protective action on N cultures. Conditioned medium from N or meningeal fibroblast cultures, either with or without VIP treatment, did not prevent TTX-mediated cell death in N test cultures. These data indicate that VIP increases the availability of neurotrophic survival-promoting substances derived from nonneuronal cultures, the most likely source being astroglial cells. This study suggests that VIP has a role in mediating a neuron-glia-neuron interaction that influences the trophic regulation of neuronal survival.
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Watanabe, Mutsufusa, Kaoru Takahashi, Kayoko Tomizawa, Hidehiro Mizusawa, and Hiroshi Takahashi. "Developmental regulation of Ubc9 in the rat nervous system." Acta Biochimica Polonica 55, no. 4 (November 28, 2008): 681–86. http://dx.doi.org/10.18388/abp.2008_3027.
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The SUMO-conjugating enzyme Ubc9 is an essential enzyme in the SUMO (small ubiquitin-related modifier) protein modification system. Although sumoylation, covalent modification of cellular proteins by SUMO, is considered to regulate various cellular processes, and many substrates for sumoylation have been identified recently, the regulation of Ubc9 expression has not been examined in detail. We analyzed the expression of Ubc9 during rat brain development at the mRNA and protein levels. Northern and Western blot analyses revealed that expression of Ubc9 and SUMO-1 was developmentally regulated, while that of the ubiquitin-conjugating enzyme UbcH7 did not change so dramatically. In situ hybridization analysis revealed that the expression of Ubc9 was high in neuronal stem cells and moderate in differentiated neurons at embryonic stages. In the adult brain, moderate expression was observed in subsets of neurons, such as the dentate granular neurons and pyramidal neurons in the hippocampal formation and the large pyramidal neurons in the cerebral cortex. These results suggest that the Ubc9-SUMO system might participate in the proliferation and differentiation of neuronal cells in the developing brain and in neuronal plasticity in the adult brain.
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Lai, James C. K. "Oxidative metabolism in neuronal and non-neuronal mitochondria." Canadian Journal of Physiology and Pharmacology 70, S1 (May 15, 1992): S130—S137. http://dx.doi.org/10.1139/y92-254.
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Methodological advances have allowed the isolation of two populations of synaptic (SM and SM2) and two populations of nonsynaptic (A and B) mitochondria from rat forebrain. All four populations of brain mitochondria are metabolically active and essentially free from nonmitochondrial contaminants. They (SM, SM2, A, and B) can oxidize a variety of substrates; the best substrate is pyruvate. With pyruvate as the substrate, the respiratory control ratios (i.e., state 3/state 4) in all four populations are routinely >6. Results from numerous enzyme activity measurements provide strong support for the hypothesis that brain mitochondria are very heterogeneous with respect to their enzyme contents and that the enzymatic activities in a particular population of mitochondria, be they synaptic or nonsynaptic, differ from those in another population of mitochondria derived from either the same or another brain region. The major methodological advances in brain mitochondrial isolation greatly facilitate metabolic studies. For example, we have demonstrated that the K+ stimulation of brain mitochondrial pyruvate oxidation is mediated through a K+-induced elevation of the activation state of the pyruvate dehydrogenase complex and the K+ stimulation of the flux through the pyruvate dehydrogenase complex. Our previous and ongoing studies using primary cultures of hypothalamic neurons and astrocytes are consistent with the proposal that brain cells are heterogeneous with respect to their capabilities in energy metabolism. I can envisage that in the not-so-distant future, one could adapt these preparations of cells as the starting material for the isolation of mitochondria of known cellular origin for metabolic studies.Key words: heterogeneity of brain mitochondria, regulation of intermediary metabolism.
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Fraser, C. L., and R. A. Swanson. "Female sex hormones inhibit volume regulation in rat brain astrocyte culture." American Journal of Physiology-Cell Physiology 267, no. 4 (October 1, 1994): C909—C914. http://dx.doi.org/10.1152/ajpcell.1994.267.4.c909.
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To determine whether sex steroids play any role in the increased morbidity associated with acute symptomatic hyponatremia in menstruant females, we studied the actions of estradiol, progesterone, and testosterone on regulatory volume decrease (RVD) of brain astrocytes in culture. To determine intracellular space with the use of 3-O-[methyl-D-3H] glucose, cells were cultured in media containing either estradiol or progesterone. Those treated with ouabain were unable to regulate volume normally, whereas testosterone-treated cells displayed normal RVD. After 15 s of hypotonic exposure, control cell volume and 100 nM testosterone-treated cell volume increased by 26 and 31%, respectively. Cell volume in control cells changed from 1.74 +/- 0.24 to 2.41 +/- 0.28 microliters/mg protein. At the same time, cells treated with either 10 nM estradiol or 10 nM progesterone significantly (P < 0.01) increased their volume by 129 and 90%, respectively. Both the antiestrogen agent tamoxifen and the antiprogesterone agent mifepristone (RU-486) blocked the effects of estradiol and progesterone. The Na-K-ATPase pump, which plays an important role in cell RVD, was significantly (P < 0.03) inhibited by 32 and 21% in estradiol- and progesterone-treated cells, but significantly (P < 0.001) stimulated (49%) by testosterone treatment. Taken together, these results provide a possible explanation for the increased morbidity associated with acute symptomatic hyponatremia in menstruant females.
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Eyo, Ukpong B., and Long-Jun Wu. "Bidirectional Microglia-Neuron Communication in the Healthy Brain." Neural Plasticity 2013 (2013): 1–10. http://dx.doi.org/10.1155/2013/456857.
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Unlike other resident neural cells that are of neuroectodermal origin, microglia are resident neural cells of mesodermal origin. Traditionally recognized for their immune functions during disease, new roles are being attributed to these cells in the development and maintenance of the central nervous system (CNS) including specific communication with neurons. In this review, we highlight some of the recent findings on the bidirectional interaction between neurons and microglia. We discuss these interactions along two lines. First, we review data that suggest that microglial activity is modulated by neuronal signals, focusing on evidence that (i) neurons are capable of regulating microglial activation state and influence basal microglial activities; (ii) classic neurotransmitters affect microglial behavior; (iii) chemotactic signals attract microglia during acute neuronal injury. Next, we discuss some of the recent data on how microglia signal to neurons. Signaling mechanisms include (i) direct physical contact of microglial processes with neuronal elements; (ii) microglial regulation of neuronal synapse and circuit by fractalkine, complement, and DAP12 signaling. In addition, we discuss the use of microglial depletion strategies in studying the role of microglia in neuronal development and synaptic physiology. Deciphering the mechanisms of bidirectional microglial-neuronal communication provides novel insights in understanding microglial function in both the healthy and diseased brain.
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Maffezzini, Camilla, Javier Calvo-Garrido, Anna Wredenberg, and Christoph Freyer. "Metabolic regulation of neurodifferentiation in the adult brain." Cellular and Molecular Life Sciences 77, no. 13 (January 7, 2020): 2483–96. http://dx.doi.org/10.1007/s00018-019-03430-9.
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AbstractUnderstanding the mechanisms behind neurodifferentiation in adults will be an important milestone in our quest to identify treatment strategies for cognitive disorders observed during our natural ageing or disease. It is now clear that the maturation of neural stem cells to neurones, fully integrated into neuronal circuits requires a complete remodelling of cellular metabolism, including switching the cellular energy source. Mitochondria are central for this transition and are increasingly seen as the regulatory hub in defining neural stem cell fate and neurodevelopment. This review explores our current knowledge of metabolism during adult neurodifferentiation.
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Robledinos-Antón, Natalia, Maribel Escoll, Kun-Liang Guan, and Antonio Cuadrado. "TAZ Represses the Neuronal Commitment of Neural Stem Cells." Cells 9, no. 10 (October 2, 2020): 2230. http://dx.doi.org/10.3390/cells9102230.
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The mechanisms involved in regulation of quiescence, proliferation, and reprogramming of Neural Stem Progenitor Cells (NSPCs) of the mammalian brain are still poorly defined. Here, we studied the role of the transcriptional co-factor TAZ, regulated by the WNT and Hippo pathways, in the homeostasis of NSPCs. We found that, in the murine neurogenic niches of the striatal subventricular zone and the dentate gyrus granular zone, TAZ is highly expressed in NSPCs and declines with ageing. Moreover, TAZ expression is lost in immature neurons of both neurogenic regions. To characterize mechanistically the role of TAZ in neuronal differentiation, we used the midbrain-derived NSPC line ReNcell VM to replicate in a non-animal model the factors influencing NSPC differentiation to the neuronal lineage. TAZ knock-down and forced expression in NSPCs led to increased and reduced neuronal differentiation, respectively. TEADs-knockdown indicated that these TAZ co-partners are required for the suppression of NSPCs commitment to neuronal differentiation. Genetic manipulation of the TAZ/TEAD system showed its participation in transcriptional repression of SOX2 and the proneuronal genes ASCL1, NEUROG2, and NEUROD1, leading to impediment of neurogenesis. TAZ is usually considered a transcriptional co-activator promoting stem cell proliferation, but our study indicates an additional function as a repressor of neuronal differentiation.
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Gaitanou, Maria, Katerina Segklia, and Rebecca Matsas. "Cend1, a Story with Many Tales: From Regulation of Cell Cycle Progression/Exit of Neural Stem Cells to Brain Structure and Function." Stem Cells International 2019 (May 2, 2019): 1–16. http://dx.doi.org/10.1155/2019/2054783.
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Neural stem/precursor cells (NPCs) generate the large variety of neuronal phenotypes comprising the adult brain. The high diversity and complexity of this organ have its origin in embryonic life, during which NPCs undergo symmetric and asymmetric divisions and then exit the cell cycle and differentiate to acquire neuronal identities. During these processes, coordinated regulation of cell cycle progression/exit and differentiation is essential for generation of the appropriate number of neurons and formation of the correct structural and functional neuronal circuits in the adult brain. Cend1 is a neuronal lineage-specific modulator involved in synchronization of cell cycle exit and differentiation of neuronal precursors. It is expressed all along the neuronal lineage, from neural stem/progenitor cells to mature neurons, and is associated with the dynamics of neuron-generating divisions. Functional studies showed that Cend1 has a critical role during neurogenesis in promoting cell cycle exit and neuronal differentiation. Mechanistically, Cend1 acts via the p53-dependent/Cyclin D1/pRb signaling pathway as well as via a p53-independent route involving a tripartite interaction with RanBPM and Dyrk1B. Upon Cend1 function, Notch1 signaling is suppressed and proneural genes such as Mash1 and Neurogenins 1/2 are induced. Due to its neurogenic activity, Cend1 is a promising candidate therapeutic gene for brain repair, while theCend1minimal promoter is a valuable tool for neuron-specific gene delivery in the CNS. Mice withCend1genetic ablation display increased NPC proliferation, decreased migration, and higher levels of apoptosis during development. As a result, they show in the adult brain deficits in a range of motor and nonmotor behaviors arising from irregularities in cerebellar cortex lamination and impaired Purkinje cell differentiation as well as a paucity in GABAergic interneurons of the cerebral cortex, hippocampus, and amygdala. Taken together, these studies highlight the necessity for Cend1 expression in the formation of a structurally and functionally normal brain.
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Wood, Ian C., Nicola K. Gray, and Lesley Jones. "Gene Expression in Neuronal Disease." Biochemical Society Transactions 37, no. 6 (November 19, 2009): 1261–62. http://dx.doi.org/10.1042/bst0371261.
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The brain is the most complex organ of the body and it contains the greatest diversity of cell types. Collectively, the cells within the brain express the greatest number of genes encoded within our genome. Inappropriate gene expression within these cells plays a fundamental role in many neuronal diseases. Illuminating the mechanisms responsible for gene expression is key to understanding these diseases. Because of the complexity, however, there is still much to understand about the mechanisms responsible for gene expression in the brain. There are many steps required for a protein to be generated from a gene, and groups who focus on gene expression normally study a single step such as regulation of transcription, mechanisms of RNA processing or control of translation. To address this, experts were brought together at the Gene Expression in Neuronal Disease meeting in Cardiff. This forum provided the latest insights into specific stages of gene expression in the brain and encompassed the complete pathway from DNA to protein. The present article summarizes the meeting talks and related papers in this issue of Biochemical Society Transactions.
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Strange, K., R. Morrison, C. W. Heilig, S. DiPietro, and S. R. Gullans. "Upregulation of inositol transport mediates inositol accumulation in hyperosmolar brain cells." American Journal of Physiology-Cell Physiology 260, no. 4 (April 1, 1991): C784—C790. http://dx.doi.org/10.1152/ajpcell.1991.260.4.c784.
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Attempts to understand brain volume regulation have been greatly hampered by the structural complexity of the mammalian central nervous system, indicating a need for the investigation of cultured brain cell lines whose behavior reflects that observed in situ. We demonstrate here that rat C6 glioma cells exhibit a pattern of hyperosmolar volume regulation qualitatively similar to that of the intact brain. Chronic (2-6 days) acclimation of C6 cells to high NaCl media (440 or 590 mosM) resulted in a 46-133 mM increase in cellular inositol, a known major brain osmolyte. C6 cells exposed acutely to 440 mosM medium shrank abruptly and then underwent a complete regulatory volume increase (RVI) within 4 h. Inositol levels began to increase after 10 h of hyperosmolar stress and reached maximal values by 24 h, suggesting that RVI is initially mediated by inorganic ion uptake. [3H]inositol uptake measurements revealed a sevenfold stimulation of phlorizin-inhibitable inositol transport in hyperosmotic cells. The enhancement of inositol transport paralleled the rise in cellular inositol content. Phlorizin reduced inositol accumulation in hyperosmolar cells by 44%. Our studies provide the first demonstration of RVI and organic osmolyte accumulation in a cultured brain cell line.
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Girdhar, Kiran, Gabriel Hoffman, Panagiotis Roussos, Schahram Akbarian, and Pamela Sklar. "Gene Regulation As A Function of Epigenetic Marks (H3K4ME3, H3K27AC) And Cell Types (Neuronal And Non Neuronal Cells) In Human Brain." European Neuropsychopharmacology 27 (2017): S423. http://dx.doi.org/10.1016/j.euroneuro.2016.09.475.
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Grasset, Estelle, and Remy Burcelin. "The gut microbiota to the brain axis in the metabolic control." Reviews in Endocrine and Metabolic Disorders 20, no. 4 (October 28, 2019): 427–38. http://dx.doi.org/10.1007/s11154-019-09511-1.
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Abstract The regulation of glycemia is under a tight neuronal detection of glucose levels performed by the gut-brain axis and an efficient efferent neuronal message sent to the peripheral organs, as the pancreas to induce insulin and inhibit glucagon secretions. The neuronal detection of glucose levels is performed by the autonomic nervous system including the enteric nervous system and the vagus nerve innervating the gastro-intestinal tractus, from the mouth to the anus. A dysregulation of this detection leads to the one of the most important current health issue around the world i.e. diabetes mellitus. Furthemore, the consequences of diabetes mellitus on neuronal homeostasis and activities participate to the aggravation of the disease establishing a viscious circle. Prokaryotic cells as bacteria, reside in our gut. The strong relationship between prokaryotic cells and our eukaryotic cells has been established long ago, and prokaryotic and eukaryotic cells in our body have evolved synbiotically. For the last decades, studies demonstrated the critical role of the gut microbiota on the metabolic control and how its shift can induce diseases such as diabetes. Despite an important increase of knowledge, few is known about 1) how the gut microbiota influences the neuronal detection of glucose and 2) how the diabetes mellitus-induced gut microbiota shift observed participates to the alterations of autonomic nervous system and the gut-brain axis activity.
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Xiong, Yuqing, Yun Zhang, Shunbin Xiong, and Abie E. Williams-Villalobo. "A Glance of p53 Functions in Brain Development, Neural Stem Cells, and Brain Cancer." Biology 9, no. 9 (September 11, 2020): 285. http://dx.doi.org/10.3390/biology9090285.
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p53 is one of the most intensively studied tumor suppressors. It transcriptionally regulates a broad range of genes to modulate a series of cellular events, including DNA damage repair, cell cycle arrest, senescence, apoptosis, ferroptosis, autophagy, and metabolic remodeling, which are fundamental for both development and cancer. This review discusses the role of p53 in brain development, neural stem cell regulation and the mechanisms of inactivating p53 in gliomas. p53 null or p53 mutant mice show female biased exencephaly, potentially due to X chromosome inactivation failure and/or hormone-related gene expression. Oxidative cellular status, increased PI3K/Akt signaling, elevated ID1, and metabolism are all implicated in p53-loss induced neurogenesis. However, p53 has also been shown to promote neuronal differentiation. In addition, p53 mutations are frequently identified in brain tumors, especially glioblastomas. Mechanisms underlying p53 inactivation in brain tumor cells include disruption of p53 protein stability, gene expression and transactivation potential as well as p53 gene loss or mutation. Loss of p53 function and gain-of-function of mutant p53 are both implicated in brain development and tumor genesis. Further understanding of the role of p53 in the brain may provide therapeutic insights for brain developmental syndromes and cancer.
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Mountian, I., P. E. Declercq, and W. Van Driessche. "Volume regulation in rat brain glial cells: lack of a substantial contribution of free amino acids." American Journal of Physiology-Cell Physiology 270, no. 5 (May 1, 1996): C1319—C1325. http://dx.doi.org/10.1152/ajpcell.1996.270.5.c1319.
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Volume regulation of C6 glioma cells was studied while the bath osmolality was reduced from 300 to 150 mosmol/kg. Exposure to a hyposmotic challenge elicited a typical regulatory volume decrease (RVD). No regulatory volume increase was observed upon restoration of isosmotic conditions. During a second subsequent hyposmotic challenge, the cells did not respond with RVD. High extracellular K+ concentration and the K+ channel blockers Ba2+ and quinine inhibited the RVD. RVD was abolished after Cl- was replaced by gluconate and by the Cl- channel blocker 5-nitro-2(3-phenylpropylamino)benzoic acid. Amino acid (AA) concentration in cell and perfusate was determined. In control, cell content was only 26 mmol/l. Hypotonicity increased the efflux of AA from 0.14 to 0.60 mmol/min. During the second hyposmotic challenge, the release was 0.32 mmol/min. The data show that C6 cells adjust their volume under hyposmotic conditions but lose the ability to restore their volume during a subsequent hyposmotic treatment. K+ and Cl- are the main osmolytes involved in volume adjustment through conductive pathways. AA do not contribute substantially to cell volume regulation.
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Pasantes-Morales, H., S. Alavez, R. S�nchez Olea, and J. Mor�n. "Contribution of organic and inorganic osmolytes to volume regulation in rat brain cells in culture." Neurochemical Research 18, no. 4 (April 1993): 445–52. http://dx.doi.org/10.1007/bf00967248.
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Yu, Chiun-Chieh, Hsiu-Ling Chen, Meng-Hsiang Chen, Cheng-Hsien Lu, Nai-Wen Tsai, Chih-Cheng Huang, Yung-Yee Chang, et al. "Vascular Inflammation Is a Risk Factor Associated with Brain Atrophy and Disease Severity in Parkinson’s Disease: A Case-Control Study." Oxidative Medicine and Cellular Longevity 2020 (July 14, 2020): 1–12. http://dx.doi.org/10.1155/2020/2591248.
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Introduction. Systemic inflammation with elevated oxidative stress causing neuroinflammation is considered a major factor in the pathogenesis of Parkinson’s disease (PD). The interface between systemic circulation and the brain parenchyma is the blood-brain barrier (BBB), which also plays a role in maintaining neurovascular homeostasis. Vascular cell adhesion molecule-1 (VCAM-1) and microRNAs (miRNAs) regulate brain vessel endothelial function, neoangiogenesis, and, in turn, neuronal homeostasis regulation, such that their dysregulation can result in neurodegeneration, such as gray matter atrophy, in PD. Objective. Our aim was to evaluate the associations among specific levels of gray matter atrophy, peripheral vascular adhesion molecules, miRNAs, and clinical disease severity in order to achieve a clearer understanding of PD pathogenesis. Methods. Blood samples were collected from 33 patients with PD and 27 healthy volunteers, and the levels of VCAM-1 and several miRNAs in those samples were measured. Voxel-based morphometry (VBM) analysis was performed using 3 T magnetic resonance imaging (MRI) and SPM (Statistical Parametric Mapping software program). The associations among the vascular parameter, miRNAs, gray matter volume, and clinical disease severity measurements were evaluated by partial correlation analysis. Results. The levels of VCAM-1, miRNA-22, and miRNA-29a expression were significantly elevated in the PD patients. The gray matter volume atrophy in the left parahippocampus, bilateral posterior cingulate gyrus, fusiform gyrus, left temporal gyrus, and cerebellum was significantly correlated with increased clinical disease severity, the upregulation of miRNA levels, and increased vascular inflammation. Conclusion. Patients with PD seem to have abnormal levels of vascular inflammatory markers and miRNAs in the peripheral circulation, and these levels are correlated with specific brain volume changes. This study reinforces the associations among peripheral inflammation, the BBB interface, and gray matter atrophy in PD and further demonstrates that BBB dysfunction with neurovascular impairment may play an important role in PD progression.
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Pak, Toni R., Wilson C. J. Chung, Laura R. Hinds, and Robert J. Handa. "Estrogen Receptor-β Mediates Dihydrotestosterone-Induced Stimulation of the Arginine Vasopressin Promoter in Neuronal Cells." Endocrinology 148, no. 7 (July 1, 2007): 3371–82. http://dx.doi.org/10.1210/en.2007-0086.
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Arginine vasopressin (AVP) is a neuropeptide involved in the regulation of fluid balance, stress, circadian rhythms, and social behaviors. In the brain, AVP is tightly regulated by gonadal steroid hormones in discrete regions with gonadectomy abolishing and testosterone replacement restoring normal AVP expression in adult males. Previous studies demonstrated that 17β-estradiol, a primary metabolite of testosterone, is responsible for restoring most of the AVP expression in the brain after castration. However, 5α-dihydrotestosterone (DHT) has also been shown to play a role in the regulation of AVP expression, thus implicating the involvement of both androgen and estrogen receptors (ER). Furthermore, DHT, through its conversion to 5α-androstane-3β,17β-diol, has been shown to modulate estrogen response element-mediated promoter activity through an ER pathway. The present study addressed two central hypotheses: 1) that androgens directly modulate AVP promoter activity and 2) the effect is mediated by an estrogen or androgen receptor pathway. To that end, we overexpressed androgen receptor, ERβ, and ERβ splice variants in a neuronal cell line and measured AVP promoter activity using a firefly luciferase reporter assay. Our results demonstrate that DHT and its metabolite 5α-androstane-3β,17β-diol stimulate AVP promoter activity through ERβ in a neuronal cell line.
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Ke, Yuehai, Eric E. Zhang, Kazuki Hagihara, Dongmei Wu, Yuhong Pang, Rüdiger Klein, Tom Curran, Barbara Ranscht, and Gen-Sheng Feng. "Deletion of Shp2 in the Brain Leads to Defective Proliferation and Differentiation in Neural Stem Cells and Early Postnatal Lethality." Molecular and Cellular Biology 27, no. 19 (July 23, 2007): 6706–17. http://dx.doi.org/10.1128/mcb.01225-07.
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ABSTRACT The intracellular signaling controlling neural stem/progenitor cell (NSC) self-renewal and neuronal/glial differentiation is not fully understood. We show here that Shp2, an introcellular tyrosine phosphatase with two SH2 domains, plays a critical role in NSC activities. Conditional deletion of Shp2 in neural progenitor cells mediated by Nestin-Cre resulted in early postnatal lethality, impaired corticogenesis, and reduced proliferation of progenitor cells in the ventricular zone. In vitro analyses suggest that Shp2 mediates basic fibroblast growth factor signals in stimulating self-renewing proliferation of NSCs, partly through control of Bmi-1 expression. Furthermore, Shp2 regulates cell fate decisions, by promoting neurogenesis while suppressing astrogliogenesis, through reciprocal regulation of the Erk and Stat3 signaling pathways. Together, these results identify Shp2 as a critical signaling molecule in coordinated regulation of progenitor cell proliferation and neuronal/astroglial cell differentiation.