Phosphorylation of HSP27 and synthesis of 14-3-3ε are parallel responses to hyperosmotic stress in the hippocampus

Niswander, Julie M.; Dokas, Linda A.

doi:10.1016/j.brainres.2006.07.119

Cited by 14 publications

(12 citation statements)

References 64 publications

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“…Brain slices maintain the tissue cytoarchitecture and extracellular matrix connections well preserved, thus allowing an in vitro microenvironment where the interactions between neuronal and glial cells are maintained closely to the in vivo situation [21,39,50]. Acute hippocampal slices (1-3 h) have been used for a diversity of in vitro studies including molecular mechanisms involved in the neurotoxicity in response to osmotic stress, heavy metals exposition and glucose/oxygen deprivation [22][23][24][25]. However, this model failed to be used for analysis of apoptotic features.…”

Section: Discussionmentioning

confidence: 99%

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Glutamate-induced Toxicity in Hippocampal Slices Involves Apoptotic Features and p38MAPK Signaling

et al. 2007

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Glutamate excitotoxicity may culminate with neuronal and glial cell death. Glutamate induces apoptosis in vivo and in cell cultures. However, glutamate-induced apoptosis and the signaling pathways related to glutamate-induced cell death in acute hippocampal slices remain elusive. Hippocampal slices exposed to 1 or 10 mM glutamate for 1 h and evaluated after 6 h, showed reduced cell viability, without altering membrane permeability. This action of glutamate was accompanied by cytochrome c release, caspase-3 activation and DNA fragmentation. Glutamate at low concentration (10 microM) induced caspase-3 activation and DNA fragmentation, but it did not cause cytochrome c release and, it did not alter the viability of slices. Glutamate-induced impairment of hippocampal cell viability was completely blocked by MK-801 (non-competitive antagonist of NMDA receptors) and GAMS (antagonist of KA/AMPA glutamate receptors). Regarding intracellular signaling pathways, glutamate-induced cell death was not altered by a MEK1 inhibitor, PD98059. However, the p38 MAPK inhibitor, SB203580, prevented glutamate-induced cell damage. In the present study we have shown that glutamate induces apoptosis in hippocampal slices and it causes an impairment of cell viability that was dependent of ionotropic and metabotropic receptors activation and, may involve the activation of p38 MAPK pathway.

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Section: Discussionmentioning

confidence: 99%

“…The brain slice is a model that mimics closely the situation in vivo, and it has been used to characterize cellular and molecular events involved in the neural physiology [16][17][18][19] and pathology [20,21], including studies of neurotoxic and neuroprotective mechanisms [22][23][24].…”

Section: Introductionmentioning

confidence: 99%

Glutamate-induced Toxicity in Hippocampal Slices Involves Apoptotic Features and p38MAPK Signaling

et al. 2007

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“…One milliliter of whole blood was collected into tubes containing 10 U heparin/mL at predose and at 1, 2, and 6 hours postdose. Samples were incubated for 1 hour at 37°C, with sorbitol (0.3 M), a known inducer of hyperosmotic stress, 14 to activate p38 MAPK signaling resulting in HSP‐27 phosphorylation. Whole‐blood samples were lysed in ice‐cold buffer containing 50 mM Tris, 300 mM NaCl, 1% v/v NP40, 0.5% deoxycholate 50 mM sodium fluoride, 1 mM sodium vanadate, and 1x fresh protease inhibitor cocktail (Sigma, St Louis, MO).…”

Section: Methodsmentioning

confidence: 99%

A Randomized, Placebo‐Controlled Study of the Effects of the p38 MAPK Inhibitor SB‐681323 on Blood Biomarkers of Inflammation in COPD Patients

Singh

Smyth

Borrill

et al. 2010

The Journal of Clinical Pharma

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The p38 mitogen-activated protein kinase (MAPK) signaling upregulates inflammation and is known to be increased in chronic obstructive pulmonary disease (COPD). The authors assessed the pharmacology of the novel p38 MAPK inhibitor SB-681323 using blood biomarkers in COPD. Seventeen COPD patients (forced expiratory volume in 1 second 50%-80% predicted) using short-acting bronchodilators participated in a double-blind, double-dummy, randomized, crossover study. Patients received single oral doses of SB-681323 7.5 mg and 25 mg, prednisolone 10 mg and 30 mg, and placebo. Blood was obtained predose and at 1, 2, 6, and 24 hours postdose. Whole-blood sorbitol-induced phosphorylated (p) heat shock protein (HSP) 27 levels as a marker of p38 pathway activation and lipopolysaccharide-induced tumor necrosis factor (TNF)-alpha production were assessed. Both doses of SB-681323, but not prednisolone, significantly (P < .0001) reduced weighted mean (WM) pHSP27 (0-6 hours) by 58% compared with placebo. WM TNF-alpha production (0-24 hours) was significantly reduced compared with placebo by SB-681323 25 mg (40%, P = .005) and 7.5 mg (33.4%, P = .02), while prednisolone 30 mg and 10 mg caused 81.5% and 58.2% suppression, respectively (both P < .0001). SB-681323 inhibited the p38 MAPK pathway to a greater degree than prednisolone did. SB-681323 inhibited TNF-alpha production. SB-681323 is a potent p38 MAPK inhibitor that potentially suppresses inflammation in COPD.

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“…IVD). Thus activation of either ERK1/2 or ERK5 can elicit disruption of the actin cytoskeleton (44), and shrinkage-induced p38 MAPK activation was directly shown to be upstream of HSP27 phosphorylation in the hippocampus (726). Moreover, MEKK4, which is upstream of JNK and p38 MAPK activation by many stimuli, was shown to be important for actin recovery after osmotic shock in mammalian cells (57).…”

Section: Roles Of Mapks In the Response To Osmotic Volume Perturbationsmentioning

confidence: 99%

Physiology of Cell Volume Regulation in Vertebrates

Hoffmann

Lambert²,

Pedersen³

2009

Physiological Reviews

1,306

1,677

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The ability to control cell volume is pivotal for cell function. Cell volume perturbation elicits a wide array of signaling events, leading to protective (e.g., cytoskeletal rearrangement) and adaptive (e.g., altered expression of osmolyte transporters and heat shock proteins) measures and, in most cases, activation of volume regulatory osmolyte transport. After acute swelling, cell volume is regulated by the process of regulatory volume decrease (RVD), which involves the activation of KCl cotransport and of channels mediating K+, Cl−, and taurine efflux. Conversely, after acute shrinkage, cell volume is regulated by the process of regulatory volume increase (RVI), which is mediated primarily by Na+/H+exchange, Na+-K+-2Cl−cotransport, and Na+channels. Here, we review in detail the current knowledge regarding the molecular identity of these transport pathways and their regulation by, e.g., membrane deformation, ionic strength, Ca2+, protein kinases and phosphatases, cytoskeletal elements, GTP binding proteins, lipid mediators, and reactive oxygen species, upon changes in cell volume. We also discuss the nature of the upstream elements in volume sensing in vertebrate organisms. Importantly, cell volume impacts on a wide array of physiological processes, including transepithelial transport; cell migration, proliferation, and death; and changes in cell volume function as specific signals regulating these processes. A discussion of this issue concludes the review.

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Phosphorylation of HSP27 and synthesis of 14-3-3ε are parallel responses to hyperosmotic stress in the hippocampus

Cited by 14 publications

References 64 publications

Glutamate-induced Toxicity in Hippocampal Slices Involves Apoptotic Features and p38MAPK Signaling

Glutamate-induced Toxicity in Hippocampal Slices Involves Apoptotic Features and p38MAPK Signaling

A Randomized, Placebo‐Controlled Study of the Effects of the p38 MAPK Inhibitor SB‐681323 on Blood Biomarkers of Inflammation in COPD Patients

Physiology of Cell Volume Regulation in Vertebrates

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