Neuroprotective effects of (24R)-1,24-dihydroxycholecalciferol in human neuroblastoma SH-SY5Y cell line

Tetich, Magdalena; Kutner, Andrzej; Leśkiewicz, Monika; Budziszewska, Bogusława; Lasoń, Władysław

doi:10.1016/j.jsbmb.2004.03.018

Cited by 22 publications

(18 citation statements)

References 16 publications

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“…2 b), Western blot analyses were carried out to detect secretion of sPLA 2 -IIA-EGFP fusion protein into the culture media. The dose of AMPA, KA, NMDA or glutamate used in these experiments was 10 M , which is less than the toxic doses of 40 M for AMPA [68] ; 25-200 M for KA [67,69] ; 0.1-5 m M for NMDA [69,70] , and 2-100 m M for glutamate [71,72] for human neuroblastoma SH-SY5Y cells. External application of KA or AMPA resulted in increased exocytosis and release of sPLA 2 -IIA whereas NMDA did not show any significant effect ( fig.…”

Section: Discussionmentioning

confidence: 94%

Kainate Receptors Mediate Regulated Exocytosis of Secretory Phospholipase A2 in SH-SY5Y Neuroblastoma Cells

Than

Tan²,

Ong

et al. 2011

Neurosignals

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Secretory phospholipase A₂ (sPLA₂) isoforms are widely expressed in the brain and spinal cord. Group IIA sPLA₂ (sPLA₂-IIA) has been shown to stimulate exocytosis and release of neurotransmitters in neuroendocrine PC12 cells and neurons, suggesting a role of the enzyme in neuronal signaling and synaptic transmission. However, the mechanisms by which sPLA₂ is itself released, and a possible relation between glutamate receptors and sPLA₂ exocytosis, are unknown. This study was carried out to elucidate the effects of glutamate receptor agonists on exocytosis of sPLA₂-IIA in transfected SH-SY5Y neuroblastoma cells. sPLA₂-IIA enzyme was packaged in fusion-competent vesicles and released constitutively or upon stimulation, suggesting regulated secretion. The signal peptide of sPLA₂-IIA is required for its vesicular localization and exocytosis. External application of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and kainate (KA) induced vesicular exocytosis and release of sPLA₂-IIA. UBP 302, a GluR5-specific KA receptor antagonist, abolished the effect of KA, confirming the role of KA receptors in mediating sPLA₂-IIA secretion. Moreover, KA-induced sPLA₂-IIA secretion is dependent on Ca²⁺ and protein kinase C. Together, these findings provide evidence of a link between glutamate receptors and regulated sPLA₂ secretion in neurons that may play an important role in synaptic plasticity, pain transmission and neurodegenerative diseases.

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Section: Discussionmentioning

confidence: 94%

Kainate Receptors Mediate Regulated Exocytosis of Secretory Phospholipase A2 in SH-SY5Y Neuroblastoma Cells

Than

Tan²,

Ong

et al. 2011

Neurosignals

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“…Zhang et al [137] demonstrated that the up-regulation of MAPK phosphatase 1 by vitamin D inhibits the lipopolysaccharide (LPS)-induced activation of p38 and cytokine production in monocytes and macrophages. In another study, the vitamin D analog (24R)-1,24-dihydroxycholecalciferol was found to prevent neuronal damage caused by hydrogen peroxide-induced toxicity in the SH-SY5Y cell line [138]. Interestingly, the neurotoxic effects of hydrogen peroxide are dependent on JNK and p38 MAPK.…”

Section: The Non-genomic Role Of Vitamin D In Malariamentioning

confidence: 98%

The role of Vitamin D in malaria

Lương

Nguyễn

2015

J Infect Dev Ctries

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An abnormal calcium-parathyroid hormone (PTH)-vitamin D axis has been reported in patients with malaria infection. A role for vitamin D in malaria has been suggested by many studies. Genetic studies have identified numerous factors that link vitamin D to malaria, including human leukocyte antigen genes, toll-like receptors, heme oxygenase-1, angiopoietin-2, cytotoxic T lymphocyte antigen-4, nucleotide-binding oligomerization domain-like receptors, and Bcl-2. Vitamin D has also been implicated in malaria via its effects on the Bacillus CalmetteGuerin (BCG) vaccine, matrix metalloproteinases, mitogen-activated protein kinase pathways, prostaglandins, reactive oxidative species, and nitric oxide synthase. Vitamin D may be important in malaria; therefore, additional research on its role in malaria is needed.

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“…VDR is highly expressed in multiple brain regions [80] in the animal [81] and human [82] brain, particularly in the pontine-midbrain area, cerebellum, thalamus, hypothalamus, basal ganglia, hippocampus, olfactory system, and the temporal, orbital, and cingulate areas of brain cortex [83]. Mounting evidence indicates that vitamin D 3 and its receptors play an important role in the brain, ranging from neuroprotection to immunomodulation [84]; cells proliferation and differentiation [85], and plays an important role both in developing [86] and adult brain [80]. Vitamin D 3 can exert these effects since it is able to cross the blood-brain barrier and can bind to VDR within the brain [87,88].…”

Section: Cardiovascular and Cerebral Riskmentioning

confidence: 99%

“…Upon binding, VDR undergoes a conformational change to form a complex with a retinoid X receptor that controls genic expression [89,90]. More recent papers demonstrate that gestational vitamin D 3 deficiency induces long-lasting alterations in the brain structure, including changes in volume, cell proliferation and reduction in the expression of nerve growth factors (NGF), glia-derived neurotrophic factor (GDNF) and neurotrophins 3 and 4 [80,83,91]. Moreover, vitamin D 3 protects neurons against NMDA, glutamate, 6-hydroxydopamine, and reactive oxygen species [92,93].…”

Section: Cardiovascular and Cerebral Riskmentioning

confidence: 99%

“…Moreover, vitamin D 3 protects neurons against NMDA, glutamate, 6-hydroxydopamine, and reactive oxygen species [92,93]. It has been hypothesized that vitamin D 3 exerts its neuroprotective effects via the modulation of neuronal Ca 2+ homeostasis, in particular through the downregulation of the L-type voltage-sensitive Ca 2+ channel in hippocampal neurons against excitotoxic insults [80], accompanied by an increase in VDR density. Vitamin D 3 is able to inhibit proinflammatory cytokine and NOS [94] typically increased during various insults or disorders, such as ischemia and reperfusion, Alzheimer's disease, Parkinson's disease, multiple sclerosis, and experimental autoimmune encephalomyelitis.…”

Section: Cardiovascular and Cerebral Riskmentioning

confidence: 99%

See 1 more Smart Citation

Vitamin D in Oxidative Stress and Diseases

Uberti¹,

Morsanuto²,

Molinari³

2017

A Critical Evaluation of Vitamin D - Basic Overview

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The data described in this chapter consider some new information about the benefits of vitamin D 3 comparing the results obtained by the authors on the effects of vitamin D 3 during oxidative stress with other works available in the literature. In particular, vitamin D 3 can induce a concentration-dependent increase in endothelial NO production through eNOS activation consequential to the phosphorylation of p38, AKT, and ERK. Additional information obtained by the author is about the ability of vitamin D 3 to prevent the endothelial cell death through modulation of interplay between apoptosis and autophagy. This effect is obtained by inhibiting superoxide anion generation, maintaining mitochondria function and cell viability, activating survival kinases (ERK and Akt), and inducing NO production. The results also describe that vitamin D 3 causes human endothelial cell proliferation and migration in a 3-D matrix through NOdependent mechanisms. These findings support the role of vitamin D 3 in the human angiogenic process, suggesting new applications for vitamin D 3 in tissue repair and wound healing. Finally, that the authors have demonstrated the ability of vitamin D 3 to counteract negative effects of oxidative stress in brain cells. These data suggest the potential therapeutic use of vitamin D to treat or prevent degenerative brain diseases.

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Neuroprotective effects of (24R)-1,24-dihydroxycholecalciferol in human neuroblastoma SH-SY5Y cell line

Cited by 22 publications

References 16 publications

Kainate Receptors Mediate Regulated Exocytosis of Secretory Phospholipase A2 in SH-SY5Y Neuroblastoma Cells

Kainate Receptors Mediate Regulated Exocytosis of Secretory Phospholipase A2 in SH-SY5Y Neuroblastoma Cells

The role of Vitamin D in malaria

Vitamin D in Oxidative Stress and Diseases

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