Glucose deprivation decreases nitric oxide production via NADPH depletion in immunostimulated rat primary astrocytes

Young Shin Chan, Woong Choi Ji, Ryun Ryu Jae, Ho K. Kwang, Jung J. Choi, Hyun S. Kim, Hee S. Kim, Jae Chul Lee, Sun Jung Lee, Chun Kim Hyoung, Won-Ki Kim

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

We have previously reported that the production of nitric oxide (NO) in immunostimulated astrocytes was markedly decreased under glucose-deprived conditions. The present study was undertaken to find the contributing factor(s) for the decreased NO production in glucose-deprived immunostimulated astrocytes. NO production in rat primary astrocytes was stimulated for 24-48 h by cotreatment with lipopolysaccharides (1 μg/ml) and interferon-γ (100 U/ml). Decreased NO production in immunostimulated astrocytes by glucose deprivation was mimicked by the glycolytic inhibitor 2-deoxyglucose and reversed by addition of pyruvate and lactate. Glucose deprivation did not alter the expression of inducible nitric oxide synthase (iNOS) in immunostimulated astrocytes. Addition of β-NADPH, but not tetrahydrobiopterine, both of which are essential cofactors for NOS function, completely restored the NO production that was decreased in glucose-deprived immunostimulated astrocytes. Glucose deprivation and immunostimulation synergistically reduced intracellular NADPH level in astrocytes. The results indicate that glucose deprivation decreases NO production in immunostimulated astrocytes by depleting intracellular NADPH, a cofactor of iNOS.

Original languageEnglish
Pages (from-to)268-274
Number of pages7
JournalGLIA
Volume37
Issue number3
DOIs
Publication statusPublished - 2002 Mar 1
Externally publishedYes

Fingerprint

NADP
Astrocytes
Nitric Oxide
Glucose
Nitric Oxide Synthase Type II
Deoxyglucose
Pyruvic Acid
Interferons
Lipopolysaccharides
Immunization
Lactic Acid

Keywords

  • Cell death
  • Cofactor
  • Glutathione
  • iNOS
  • Tetrahydrobiopterine

ASJC Scopus subject areas

  • Immunology

Cite this

Glucose deprivation decreases nitric oxide production via NADPH depletion in immunostimulated rat primary astrocytes. / Chan, Young Shin; Ji, Woong Choi; Jae, Ryun Ryu; Kwang, Ho K.; Choi, Jung J.; Kim, Hyun S.; Kim, Hee S.; Lee, Jae Chul; Lee, Sun Jung; Hyoung, Chun Kim; Kim, Won-Ki.

In: GLIA, Vol. 37, No. 3, 01.03.2002, p. 268-274.

Research output: Contribution to journalArticle

Chan, YS, Ji, WC, Jae, RR, Kwang, HK, Choi, JJ, Kim, HS, Kim, HS, Lee, JC, Lee, SJ, Hyoung, CK & Kim, W-K 2002, 'Glucose deprivation decreases nitric oxide production via NADPH depletion in immunostimulated rat primary astrocytes', GLIA, vol. 37, no. 3, pp. 268-274. https://doi.org/10.1002/glia.10032
Chan, Young Shin ; Ji, Woong Choi ; Jae, Ryun Ryu ; Kwang, Ho K. ; Choi, Jung J. ; Kim, Hyun S. ; Kim, Hee S. ; Lee, Jae Chul ; Lee, Sun Jung ; Hyoung, Chun Kim ; Kim, Won-Ki. / Glucose deprivation decreases nitric oxide production via NADPH depletion in immunostimulated rat primary astrocytes. In: GLIA. 2002 ; Vol. 37, No. 3. pp. 268-274.
@article{992546afdef74d6dac3c1831330959c3,
title = "Glucose deprivation decreases nitric oxide production via NADPH depletion in immunostimulated rat primary astrocytes",
abstract = "We have previously reported that the production of nitric oxide (NO) in immunostimulated astrocytes was markedly decreased under glucose-deprived conditions. The present study was undertaken to find the contributing factor(s) for the decreased NO production in glucose-deprived immunostimulated astrocytes. NO production in rat primary astrocytes was stimulated for 24-48 h by cotreatment with lipopolysaccharides (1 μg/ml) and interferon-γ (100 U/ml). Decreased NO production in immunostimulated astrocytes by glucose deprivation was mimicked by the glycolytic inhibitor 2-deoxyglucose and reversed by addition of pyruvate and lactate. Glucose deprivation did not alter the expression of inducible nitric oxide synthase (iNOS) in immunostimulated astrocytes. Addition of β-NADPH, but not tetrahydrobiopterine, both of which are essential cofactors for NOS function, completely restored the NO production that was decreased in glucose-deprived immunostimulated astrocytes. Glucose deprivation and immunostimulation synergistically reduced intracellular NADPH level in astrocytes. The results indicate that glucose deprivation decreases NO production in immunostimulated astrocytes by depleting intracellular NADPH, a cofactor of iNOS.",
keywords = "Cell death, Cofactor, Glutathione, iNOS, Tetrahydrobiopterine",
author = "Chan, {Young Shin} and Ji, {Woong Choi} and Jae, {Ryun Ryu} and Kwang, {Ho K.} and Choi, {Jung J.} and Kim, {Hyun S.} and Kim, {Hee S.} and Lee, {Jae Chul} and Lee, {Sun Jung} and Hyoung, {Chun Kim} and Won-Ki Kim",
year = "2002",
month = "3",
day = "1",
doi = "10.1002/glia.10032",
language = "English",
volume = "37",
pages = "268--274",
journal = "GLIA",
issn = "0894-1491",
publisher = "John Wiley and Sons Inc.",
number = "3",

}

TY - JOUR

T1 - Glucose deprivation decreases nitric oxide production via NADPH depletion in immunostimulated rat primary astrocytes

AU - Chan, Young Shin

AU - Ji, Woong Choi

AU - Jae, Ryun Ryu

AU - Kwang, Ho K.

AU - Choi, Jung J.

AU - Kim, Hyun S.

AU - Kim, Hee S.

AU - Lee, Jae Chul

AU - Lee, Sun Jung

AU - Hyoung, Chun Kim

AU - Kim, Won-Ki

PY - 2002/3/1

Y1 - 2002/3/1

N2 - We have previously reported that the production of nitric oxide (NO) in immunostimulated astrocytes was markedly decreased under glucose-deprived conditions. The present study was undertaken to find the contributing factor(s) for the decreased NO production in glucose-deprived immunostimulated astrocytes. NO production in rat primary astrocytes was stimulated for 24-48 h by cotreatment with lipopolysaccharides (1 μg/ml) and interferon-γ (100 U/ml). Decreased NO production in immunostimulated astrocytes by glucose deprivation was mimicked by the glycolytic inhibitor 2-deoxyglucose and reversed by addition of pyruvate and lactate. Glucose deprivation did not alter the expression of inducible nitric oxide synthase (iNOS) in immunostimulated astrocytes. Addition of β-NADPH, but not tetrahydrobiopterine, both of which are essential cofactors for NOS function, completely restored the NO production that was decreased in glucose-deprived immunostimulated astrocytes. Glucose deprivation and immunostimulation synergistically reduced intracellular NADPH level in astrocytes. The results indicate that glucose deprivation decreases NO production in immunostimulated astrocytes by depleting intracellular NADPH, a cofactor of iNOS.

AB - We have previously reported that the production of nitric oxide (NO) in immunostimulated astrocytes was markedly decreased under glucose-deprived conditions. The present study was undertaken to find the contributing factor(s) for the decreased NO production in glucose-deprived immunostimulated astrocytes. NO production in rat primary astrocytes was stimulated for 24-48 h by cotreatment with lipopolysaccharides (1 μg/ml) and interferon-γ (100 U/ml). Decreased NO production in immunostimulated astrocytes by glucose deprivation was mimicked by the glycolytic inhibitor 2-deoxyglucose and reversed by addition of pyruvate and lactate. Glucose deprivation did not alter the expression of inducible nitric oxide synthase (iNOS) in immunostimulated astrocytes. Addition of β-NADPH, but not tetrahydrobiopterine, both of which are essential cofactors for NOS function, completely restored the NO production that was decreased in glucose-deprived immunostimulated astrocytes. Glucose deprivation and immunostimulation synergistically reduced intracellular NADPH level in astrocytes. The results indicate that glucose deprivation decreases NO production in immunostimulated astrocytes by depleting intracellular NADPH, a cofactor of iNOS.

KW - Cell death

KW - Cofactor

KW - Glutathione

KW - iNOS

KW - Tetrahydrobiopterine

UR - http://www.scopus.com/inward/record.url?scp=0036509898&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0036509898&partnerID=8YFLogxK

U2 - 10.1002/glia.10032

DO - 10.1002/glia.10032

M3 - Article

C2 - 11857685

AN - SCOPUS:0036509898

VL - 37

SP - 268

EP - 274

JO - GLIA

JF - GLIA

SN - 0894-1491

IS - 3

ER -