Roles of Ca2+ and the Ca2+‐sensing receptor (CASR) in the expression of inducible NOS (nitric oxide synthase)‐2 and its BH4 (tetrahydrobiopterin)‐dependent activation in cytokine‐stimulated adult human astrocytes
Abstract
Since NO production by NOS‐2 made by astrocytes activated by proinflammatory cytokines contributes to the killing of neurons in variously damaged human brains, knowing the mechanisms responsible for NOS‐2 expression should contribute to developing effective therapeutics. The expression and activation of NOS‐2 in normal adult human cerebral cortical astrocytes treated with three proinflammatory cytokines, IL‐1β, TNF‐α, and IFN‐γ, are driven by two separable mechanisms. NOS‐2 expression requires a burst of p38 MAPK activity, while the activation of the resulting enzyme protein requires MEK/ERK‐dependent BH 4 (tetrahydrobiopterin) synthesis between 24 and 24.5 h after adding the cytokines to the culture medium. Here we show that NOS‐2 expression in the activated astrocytes requires that the culture medium contain 1.8 mM Ca 2+, but it is unaffected by inhibiting calcium‐sensing receptors (CASRs) with NPS 89636. However, NOS‐2 activation is inhibited by NPS 89626 during the MEK/ERK‐dependent stage between 24 and 24.5 h after adding the cytokines, and this inhibition can be overridden by exogenous BH 4. Therefore, NOS‐2 expression and the subsequent BH 4‐dependent NOS‐2‐activation in human astrocytes need 1.8 mM Ca 2+ to be in the culture medium, while NOS‐2 activation also needs functional CASRs between 24 and 24.5 h after cytokine addition. These findings raise the possibility that calcilytic drugs prevent NO‐induced damage and death of human neurons. © 2005 Wiley‐Liss, Inc.
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Interactions between Aβ42 oligomers and CaSR induce NO production/secretion and expression of NOS-2 and VEGF-A through MEK/ERK-dependent pathways, aggravating neuroinflammation.
“Moreover, interactions between Aβ42 oligomers and CaSR can also induce NO production/secretion, and expression of nitric oxide synthase-2 as well as vascular endothelial growth factor-A through activation of MEK/ERK-dependent pathways, thereby aggravating neuroinflammation [394, 402].”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [394]
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Janssen, V., Kamel, S., Slama, M., Arab, O. A., Brazier, M., Mentaverri, R., & Mary, A. (2026) · Inflammation Research · doi:10.1007/s00011-026-02227-4 · Cited by 1 · see citing works
Wu, C. (2012) · eScholarship@McGill (McGill) · doi:10.82308/22089
Regulation of the calcium-sensing receptor by amyloid-beta-42 : implications for Alzheimer's disease
Freba, J. Z. (2013) · Submitted in <b>2013</b>
- Authors
- Dal Pra, I., Chiarini, A., Nemeth, E. F., Armato, U., & Whitfield, J. F.
- Affiliations
- University of Verona (IT)
- Institute for Biological Sciences (CA)
- Corresponding author
- Whitfield, James F.
- Venue
- Journal of Cellular Biochemistry
- Publisher
- Wiley
- Published
- 2005-07-28
- Volume
- 96
- Issue
- 2
- Pages
- 428-438
- ISSN
- 0730-2312 (ISSN-L)
- 1097-4644
- OpenAlex
- W1971314625
- Cited by
- 47
- References
- 58
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 2 · 2023: 1 · 2022: 2 · 2020: 3 · 2019: 4 · 2018: 1 · 2017: 3 · 2016: 6 · 2015: 1 · 2014: 3 · 2013: 3 · 2012: 4
- FWCI
- 0.60
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Cellular Biochemistry (publishedVersion)
- PubMed (publishedVersion)
- NPARC (submittedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Keywords
- nitric oxide synthase 2, calcium-sensing receptor, calcium signaling, tetrahydrobiopterin, astrocytes, inflammatory cytokines, IL-1β, TNF-α, interferon-gamma, p38 MAPK, MEK/ERK signaling, neuroprotection, cerebral cortex
- MeSH terms
- Adult, Aging, Astrocytes, Biopterins, Calcium, Cations, Divalent, Enzyme Activation, Humans, Nitric Oxide, Gene Expression Regulation, Enzymologic, Cytokines, Receptors, Calcium-Sensing, Extracellular Signal-Regulated MAP Kinases, Cell Proliferation
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