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Cited by 129Heme Oxygenase-1 and Carbon MonoxideMultiple Sclerosis Research StudiesIron Metabolism and Disorders

The DOI matches its Crossref record; 53 of the 54 references it cites were found in a registry or an index.

Proinflammatory cytokines promote glial heme oxygenase-1 expression and mitochondrial iron deposition: implications for multiple sclerosis

Mehindate, K., Sahlas, D. J., Frankel, D., Mawal, Y., Liberman, A., Corcos, J., Dion, S., Schipper, H. M.·2001·Journal of Neurochemistry
DOI 10.1046/j.1471-4159.2001.00354.x
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Abstract

Proinflammatory cytokines, pathological iron deposition, and oxidative stress have been implicated in the pathogenesis of multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE). HO-1 mRNA levels and mitochondrial uptake of [(55)Fe]Cl(3)-derived iron were measured in rat astroglial cultures exposed to interleukin-1beta (IL-1beta) or tumor necrosis factor-alpha (TNF-alpha) alone or in combination with the heme oxygenase-1 (HO-1) inhibitors, tin mesoporphyrin (SnMP) or dexamthasone (DEX), or interferon beta1b (INF-beta). HO-1 expression in astrocytes was evaluated by immunohistochemical staining of spinal cord tissue derived from MS and control subjects. IL-1beta or TNF-alpha promoted sequestration of non-transferrin-derived (55)Fe by astroglial mitochondria. HO-1 inhibitors, mitochondrial permeability transition pore (MTP) blockers and antioxidants significantly attenuated cytokine-related mitochondrial iron sequestration in these cells. IFN-beta decreased HO-1 expression and mitochondrial iron sequestration in IL-1beta- and TNF-alpha-challenged astroglia. The percentage of astrocytes coexpressing HO-1 in affected spinal cord from MS patients (57.3% +/- 12.8%) was significantly greater (p < 0.05) than in normal spinal cord derived from controls subjects (15.4% +/- 8.4%). HO-1 is over-expressed in MS spinal cord astroglia and may promote mitochondrial iron deposition in MS plaques. In MS, IFN-beta may attenuate glial HO-1 gene induction and aberrant mitochondrial iron deposition accruing from exposure to proinflammatory cytokines.

Overview

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Crossref · 10.1046/j.1471-4159.2001.00354.x

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Citations

Cites

Research works printed but not linked: 3

  1. 10.1016/0003-2697(87)90021-2 · DOI
  2. Paty D. W., 1998, Multiple Sclerosis, 427
  3. Trapp B. D., 1995, Cellular mechanisms of demyelination in multiple sclerosis brains, J. Neurochem., 64

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Metadata

Authors
Mehindate, K., Sahlas, D. J., Frankel, D., Mawal, Y., Liberman, A., Corcos, J., Dion, S., & Schipper, H. M.
Affiliations
  • Jewish General Hospital (CA)
  • McGill University (CA)
Corresponding author
Schipper, H. M.
ORCID
Venue
Journal of Neurochemistry
Publisher
Wiley
Published
2001-06
Volume
77
Issue
5
Pages
1386-1395
ISSN
  • 0022-3042 (ISSN-L)
  • 1471-4159
DOI
10.1046/j.1471-4159.2001.00354.x
OpenAlex
W1902487112
Cited by
129
References
54
Citations by year
2025: 1 · 2024: 4 · 2023: 5 · 2022: 1 · 2021: 1 · 2020: 4 · 2019: 2 · 2018: 3 · 2017: 7 · 2016: 2 · 2015: 5 · 2014: 7 · 2013: 3 · 2012: 3
FWCI
2.79
Type
journal article
Language
en
Open access
closed
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor, 202 d)
Locations
  • Journal of Neurochemistry (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Fonds de Recherche du Québec - Santé
  • Medical Research Council
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Heme Oxygenase-1 and Carbon Monoxide
  • Health Sciences › Medicine › Clinical Neurology › Multiple Sclerosis Research Studies
  • Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
Keywords
heme oxygenase-1, multiple sclerosis, inflammatory cytokines, IL-1β, TNF-α, astrocytes, iron sequestration, interferon-beta, experimental autoimmune encephalomyelitis, oxidative stress, mitochondrial permeability transition pore, tin mesoporphyrin, dexamethasone
MeSH terms
Animals, Cells, Cultured, Chlorides, Encephalomyelitis, Autoimmune, Experimental, Female, Ferric Compounds, Heme Oxygenase (Decyclizing), Humans, Immunohistochemistry, Interleukin-1, Iron, Iron Radioisotopes, Mitochondria, Multiple Sclerosis, Neuroglia, RNA, Messenger, Spinal Cord, Subcellular Fractions, Transferrin, Tumor Necrosis Factor-alpha, Blotting, Northern, Cytokines, Rats, Sprague-Dawley, Rats

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