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[논문] Glutamine Cooperatively Upregulates Lipopolysaccharide-Induced Nitric Oxide Production in BV2 Microglial Cells through the ERK and Nrf-2/HO-1 Signaling Pathway

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논문제목(Title)

[논문] Glutamine Cooperatively Upregulates Lipopolysaccharide-Induced Nitric Oxide Production in BV2 Microglial Cells through the ERK and Nrf-2/HO-1 Signaling Pathway

학술지명(Journal)

Antioxidants

ImpactFactor

6.313

ISSN_ISBN

EISSN: 2076-3921

학술지볼륨권호(Volume)

9

SCI구분

SCIE

초록(Abstract)

Glutamine (Gln) is a nonessential -amino acid for protein biosynthesis. However, the mechanism through which Gln regulates NO production in microglial cells is still unclear. In this study, we investigated whether the presence or absence of Gln a ects NO production in lipopolysaccharide (LPS)-stimulated BV2 microglial cells. Our data revealed that Gln depletion
decreased cell viability accompanied by mild cytotoxicity, and blocked LPS-induced NO production
concomitant with a significant decrease in inducible NO synthase (iNOS) expression. Additionally, Gln depletion for 24 h blocked the restoration of LPS-mediated NO production in the presence of Gln, suggesting that Gln depletion caused long-term immune deprivation. In particular, sodium-coupled amino acid transporter 1 and 2 (SNAT1 and SNAT2), which are the main Gln transporters, were highly upregulated in LPS-stimulated BV2 microglial cells, in the presence of Gln accompanied by NO production. Regardless of the presence of Gln, LPS positively stimulated nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) expression, and transient Nrf2 knockdown and HO-1 inhibition stimulated LPS-induced NO production and iNOS expression; however, transient Nrf2 knockdown did not a ect SNAT1 and SNAT2 expression, indicating that Gln ransporters,
SNAT1 and SNAT2, were not regulated by Nrf2, which downregulated the HO-1-mediated NO production. Moreover, Gln depletion significantly reduced LPS-induced extracellular signal-regulated kinase (ERK) phosphorylation; furthermore, a specific ERK inhibitor, PD98059, and transient ERK knockdown attenuated LPS-stimulated NO production and iNOS expression, in the presence of Gln, accompanied by downregulation of SNAT1 and SNAT2, suggesting that the ERK signaling pathway was related to LPS-mediated NO production via SNAT1 and SNAT2. Altogether, our data indicated that extracellular Gln is vital for NO production from microglia in inflammatory conditions.

저자명(Author)

Jayasooriya, Rajapaksha Gedara Prasad Tharanga; Molagoda, Ilandarage Menu Neelaka; Dilshara, Matharage Gayani; Choi, Yung Hyun; Kim, Gi-Young;

학술지출판일자(PublicationDate)

2020-06-01

공개 및 라이선스

공개 일자

2021-12-17

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김기영
공개일자
2021-12-17
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  • Version 1 2021-02-18
Cite as
Jayasooriya, Rajapaksha Gedara Prasad Tharanga; Molagoda, Ilandarage Menu Neelaka; Dilshara, Matharage Gayani; Choi, Yung Hyun; Kim, Gi-Young;, 2020-06-01, [논문] Glutamine Cooperatively Upregulates Lipopolysaccharide-Induced Nitric Oxide Production in BV2 Microglial Cells through the ERK and Nrf-2/HO-1 Signaling Pathway
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