p38 mitogen-activated protein kinase mediates lipopolysaccharide, not interferon-γ, -induced inducible nitric oxide synthase expression in mouse BV2 microglial cells

Inn Oc Han; Ki Wan Kim; Jong Hoon Ryu; Won Ki Kim

doi:10.1016/S0304-3940(02)00218-5

p38 mitogen-activated protein kinase mediates lipopolysaccharide, not interferon-γ, -induced inducible nitric oxide synthase expression in mouse BV2 microglial cells

Inn Oc Han, Ki Wan Kim, Jong Hoon Ryu, Won Ki Kim

Research output: Contribution to journal › Article › peer-review

65 Citations (Scopus)

Abstract

The present study examined the role of mitogen-activated protein kinases (MAPKs) in inducible nitric oxide synthase (iNOS) induction by lipopolysaccharide (LPS) or interferon-γ (IFN-γ) in the murine microglial cell line BV2 cells. LPS rapidly (<2 h) induced iNOS mRNA expression whereas IFN-γ did not within 8 h after stimulation. LPS activated three MAPK subtypes, extracellular signal-regulated kinase (ERK), p38 and c-Jun N-terminal kinase (JNK) as early as 15 min after stimulation. In contrast, IFN-γ activated only ERK after 6 h of stimulation and did not alter the activity of p38 and JNK. LPS-induced iNOS expression was markedly decreased by the p38 inhibitor SB203580, but not by the MAPK or ERK kinase inhibitor PD98059. IFN-γ-induced nitric oxide (NO) generation was partially inhibited by PD98059 and SB203580 only in combination. The results demonstrate that MAPKs differentially mediate NO production by LPS- and IFN-γ in BV2 cells.

Original language	English
Pages (from-to)	9-12
Number of pages	4
Journal	Neuroscience Letters
Volume	325
Issue number	1
DOIs	https://doi.org/10.1016/S0304-3940(02)00218-5
Publication status	Published - 2002 May 31
Externally published	Yes

Bibliographical note

Funding Information:
This work was supported by a grant (#R01-1999-00101) of the Korea Science and Engineering Foundation, and the Neurobiology Research Program from the Korea Ministry of Science and Technology, Republic of Korea. I.-O. Han is the recipient of a Research Fellowship (Brain Korea 21 Project).

Keywords

Extracellular signal-regulated kinase
Inducible nitric oxide synthase
Interferon-γ
Lipopolysaccharide
Microglia
Nitric oxide
c-Jun N-terminal kinase
p38

ASJC Scopus subject areas

General Neuroscience

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10.1016/S0304-3940(02)00218-5

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title = "p38 mitogen-activated protein kinase mediates lipopolysaccharide, not interferon-γ, -induced inducible nitric oxide synthase expression in mouse BV2 microglial cells",

abstract = "The present study examined the role of mitogen-activated protein kinases (MAPKs) in inducible nitric oxide synthase (iNOS) induction by lipopolysaccharide (LPS) or interferon-γ (IFN-γ) in the murine microglial cell line BV2 cells. LPS rapidly (<2 h) induced iNOS mRNA expression whereas IFN-γ did not within 8 h after stimulation. LPS activated three MAPK subtypes, extracellular signal-regulated kinase (ERK), p38 and c-Jun N-terminal kinase (JNK) as early as 15 min after stimulation. In contrast, IFN-γ activated only ERK after 6 h of stimulation and did not alter the activity of p38 and JNK. LPS-induced iNOS expression was markedly decreased by the p38 inhibitor SB203580, but not by the MAPK or ERK kinase inhibitor PD98059. IFN-γ-induced nitric oxide (NO) generation was partially inhibited by PD98059 and SB203580 only in combination. The results demonstrate that MAPKs differentially mediate NO production by LPS- and IFN-γ in BV2 cells.",

keywords = "Extracellular signal-regulated kinase, Inducible nitric oxide synthase, Interferon-γ, Lipopolysaccharide, Microglia, Nitric oxide, c-Jun N-terminal kinase, p38",

author = "Han, {Inn Oc} and Kim, {Ki Wan} and Ryu, {Jong Hoon} and Kim, {Won Ki}",

note = "Funding Information: This work was supported by a grant (#R01-1999-00101) of the Korea Science and Engineering Foundation, and the Neurobiology Research Program from the Korea Ministry of Science and Technology, Republic of Korea. I.-O. Han is the recipient of a Research Fellowship (Brain Korea 21 Project).",

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doi = "10.1016/S0304-3940(02)00218-5",

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AU - Han, Inn Oc

AU - Kim, Ki Wan

AU - Ryu, Jong Hoon

AU - Kim, Won Ki

N1 - Funding Information: This work was supported by a grant (#R01-1999-00101) of the Korea Science and Engineering Foundation, and the Neurobiology Research Program from the Korea Ministry of Science and Technology, Republic of Korea. I.-O. Han is the recipient of a Research Fellowship (Brain Korea 21 Project).

PY - 2002/5/31

Y1 - 2002/5/31

N2 - The present study examined the role of mitogen-activated protein kinases (MAPKs) in inducible nitric oxide synthase (iNOS) induction by lipopolysaccharide (LPS) or interferon-γ (IFN-γ) in the murine microglial cell line BV2 cells. LPS rapidly (<2 h) induced iNOS mRNA expression whereas IFN-γ did not within 8 h after stimulation. LPS activated three MAPK subtypes, extracellular signal-regulated kinase (ERK), p38 and c-Jun N-terminal kinase (JNK) as early as 15 min after stimulation. In contrast, IFN-γ activated only ERK after 6 h of stimulation and did not alter the activity of p38 and JNK. LPS-induced iNOS expression was markedly decreased by the p38 inhibitor SB203580, but not by the MAPK or ERK kinase inhibitor PD98059. IFN-γ-induced nitric oxide (NO) generation was partially inhibited by PD98059 and SB203580 only in combination. The results demonstrate that MAPKs differentially mediate NO production by LPS- and IFN-γ in BV2 cells.

AB - The present study examined the role of mitogen-activated protein kinases (MAPKs) in inducible nitric oxide synthase (iNOS) induction by lipopolysaccharide (LPS) or interferon-γ (IFN-γ) in the murine microglial cell line BV2 cells. LPS rapidly (<2 h) induced iNOS mRNA expression whereas IFN-γ did not within 8 h after stimulation. LPS activated three MAPK subtypes, extracellular signal-regulated kinase (ERK), p38 and c-Jun N-terminal kinase (JNK) as early as 15 min after stimulation. In contrast, IFN-γ activated only ERK after 6 h of stimulation and did not alter the activity of p38 and JNK. LPS-induced iNOS expression was markedly decreased by the p38 inhibitor SB203580, but not by the MAPK or ERK kinase inhibitor PD98059. IFN-γ-induced nitric oxide (NO) generation was partially inhibited by PD98059 and SB203580 only in combination. The results demonstrate that MAPKs differentially mediate NO production by LPS- and IFN-γ in BV2 cells.

KW - Extracellular signal-regulated kinase

KW - Inducible nitric oxide synthase

KW - Interferon-γ

KW - Lipopolysaccharide

KW - Microglia

KW - Nitric oxide

KW - c-Jun N-terminal kinase

KW - p38

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SN - 0304-3940

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ER -

p38 mitogen-activated protein kinase mediates lipopolysaccharide, not interferon-γ, -induced inducible nitric oxide synthase expression in mouse BV2 microglial cells

Abstract

Bibliographical note

Keywords

ASJC Scopus subject areas

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