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Diminished calcium homeostasis and increased susceptibility to excitotoxicity of JS 3/16 progenitor cells after differentiation to oligodendroglia.
Glia. 2000 Aug; 31(2):165-80.GLIA

Abstract

JS 3/16, derived from passaged oligodendroglial cultures prepared from rat cerebral white matter, differentiate from progenitors (OP) into complex process-bearing, galactocerebroside-positive but myelin basic protein-negative immature oligodendrocyte-like cells (ImO) after withdrawal of trophic factors. We found that JS 3/16 ImO are markedly more susceptible than OP to cell death after sustained alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate glutamate receptor (AMPA-GluR) activation. This excitotoxicity is preceded by loss of intracellular Ca(2+) homeostasis, which is more marked in ImO than OP. We identified three factors likely to contribute to the diminished Ca(2+) homeostatic capacity of ImO. First, signal intensities of immunoreactive GluR2, GluR3, and GluR4 AMPA-GluR subunits are increased 1.3- to 2.2-fold in ImO over OP without comparable changes in RNA editing and alternative splicing. Second, transcriptional levels of genes encoding Na(+)-Ca(2+) exchanger proteins and a plasma membrane ATPase (PMCA1), which are necessary for Ca(2+) extrusion across the plasma membrane, are lower in ImO than in OP. Third, ImO have more depolarized basal mitochondrial membrane potential (Delta Psi) than OP, and Delta Psi collapses within 15 min after onset of AMPA-GluR activation in almost all ImO, but not in the majority of OP. This Delta Psi collapse limits the capacity of ImO mitochondria to buffer the rise in intracellular Ca(2+) caused by AMPA-GluR activation. The JS 3/16 line provides a valuable system for analysis of intracellular Ca(2+) homeostasis and AMPA-GluR-mediated excitotoxicity in the oligodendroglial lineage.

Authors+Show Affiliations

Neurology Research, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104, USA. takayuki@mail.med.upenn.eduNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

10878603

Citation

Itoh, T, et al. "Diminished Calcium Homeostasis and Increased Susceptibility to Excitotoxicity of JS 3/16 Progenitor Cells After Differentiation to Oligodendroglia." Glia, vol. 31, no. 2, 2000, pp. 165-80.
Itoh T, Reddy UR, Stern JL, et al. Diminished calcium homeostasis and increased susceptibility to excitotoxicity of JS 3/16 progenitor cells after differentiation to oligodendroglia. Glia. 2000;31(2):165-80.
Itoh, T., Reddy, U. R., Stern, J. L., Chen, M., Itoh, A., & Pleasure, D. (2000). Diminished calcium homeostasis and increased susceptibility to excitotoxicity of JS 3/16 progenitor cells after differentiation to oligodendroglia. Glia, 31(2), 165-80.
Itoh T, et al. Diminished Calcium Homeostasis and Increased Susceptibility to Excitotoxicity of JS 3/16 Progenitor Cells After Differentiation to Oligodendroglia. Glia. 2000;31(2):165-80. PubMed PMID: 10878603.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Diminished calcium homeostasis and increased susceptibility to excitotoxicity of JS 3/16 progenitor cells after differentiation to oligodendroglia. AU - Itoh,T, AU - Reddy,U R, AU - Stern,J L, AU - Chen,M, AU - Itoh,A, AU - Pleasure,D, PY - 2000/7/6/pubmed PY - 2000/9/23/medline PY - 2000/7/6/entrez SP - 165 EP - 80 JF - Glia JO - Glia VL - 31 IS - 2 N2 - JS 3/16, derived from passaged oligodendroglial cultures prepared from rat cerebral white matter, differentiate from progenitors (OP) into complex process-bearing, galactocerebroside-positive but myelin basic protein-negative immature oligodendrocyte-like cells (ImO) after withdrawal of trophic factors. We found that JS 3/16 ImO are markedly more susceptible than OP to cell death after sustained alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate glutamate receptor (AMPA-GluR) activation. This excitotoxicity is preceded by loss of intracellular Ca(2+) homeostasis, which is more marked in ImO than OP. We identified three factors likely to contribute to the diminished Ca(2+) homeostatic capacity of ImO. First, signal intensities of immunoreactive GluR2, GluR3, and GluR4 AMPA-GluR subunits are increased 1.3- to 2.2-fold in ImO over OP without comparable changes in RNA editing and alternative splicing. Second, transcriptional levels of genes encoding Na(+)-Ca(2+) exchanger proteins and a plasma membrane ATPase (PMCA1), which are necessary for Ca(2+) extrusion across the plasma membrane, are lower in ImO than in OP. Third, ImO have more depolarized basal mitochondrial membrane potential (Delta Psi) than OP, and Delta Psi collapses within 15 min after onset of AMPA-GluR activation in almost all ImO, but not in the majority of OP. This Delta Psi collapse limits the capacity of ImO mitochondria to buffer the rise in intracellular Ca(2+) caused by AMPA-GluR activation. The JS 3/16 line provides a valuable system for analysis of intracellular Ca(2+) homeostasis and AMPA-GluR-mediated excitotoxicity in the oligodendroglial lineage. SN - 0894-1491 UR - https://www.unboundmedicine.com/medline/citation/10878603/Diminished_calcium_homeostasis_and_increased_susceptibility_to_excitotoxicity_of_JS_3/16_progenitor_cells_after_differentiation_to_oligodendroglia_ L2 - https://medlineplus.gov/stemcells.html DB - PRIME DP - Unbound Medicine ER -