Induction of nitric oxide synthase in RAW 264.7 macrophages by lipoteichoic acid from Staphylococcus aureus: Involvement of protein kinase C- and nuclear factor-κB-dependent mechanisms

Chen Tzu Kuo, Ling Ling Chiang, Chun-Nin Lee, Ming Chih Yu, Kuan Jen Bai, Horng Mo Lee, Wen Sen Lee, Joen Rong Sheu, Chien Huang Lin

研究成果: 雜誌貢獻 › 文章

20 引文 (Scopus)

摘要

This study investigates the signaling pathway involved in inducible nitric oxide synthase (iNOS) expression and nitric oxide (NO) release caused by Staphylococcus aureus lipoteichoic acid (LTA) in RAW 264.7 macrophages. A phosphatidylcholine-phospholipase C (PC-PLC) inhibitor (D-609) and a phosphatidylinositol-phospholipase C (PI-PLC) inhibitor (U-73122) attenuated LTA-induced iNOS expression and NO release. Two PKC inhibitors (Go 6976 and Ro 31-8220), an NF-κB inhibitor (pyrrolidine dithiocarbamate; PDTC), and long-term (24 h) 12-phorbol-13-myristate acetate (PMA) treatment each also inhibited LTA-induced iNOS expression and NO release. Treatment of cells with LTA caused an increase in PKC activity; this stimulatory effect was inhibited by D-609, U-73122, or Ro 31-8220. Stimulation of cells with LTA caused IκB-α phosphorylation and IκB-α degradation in the cytosol, and translocation of p65 and p50 NF-κB from the cytosol to the nucleus. Treatment of cells with LTA caused NF-κB activation by detecting the formation of NF-κB-specific DNA-protein complexes in the nucleus; this effect was inhibited by Go 6976, Ro 31-8220, long-term PMA treatment, PDTC, L-1-tosylamido-2-phenylethyl chloromethyl ketone (TPCK), and calpain inhibitor I. These results suggest that LTA might activate PC-PLC and PI-PLC to induce PKC activation, which in turn initiates NF-κB activation, and finally induces iNOS expression and NO release in RAW 264.7 macrophages.
原文英語
頁（從 - 到）136-145
頁數10
期刊Journal of Biomedical Science
卷10
發行號1
DOIs
出版狀態已發佈 - 2003

指紋

Macrophages
Nitric Oxide Synthase
Protein Kinase C
Staphylococcus aureus
Type C Phospholipases
Nitric Oxide Synthase Type II
Nitric Oxide
Chemical activation
Myristic Acid
Tetradecanoylphorbol Acetate
Phosphatidylinositols
Phosphatidylcholines
Cytosol
Acetates
Cells
Phosphorylation
lipoteichoic acid
Ketones
Degradation
DNA

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

引用此文

Induction of nitric oxide synthase in RAW 264.7 macrophages by lipoteichoic acid from Staphylococcus aureus : Involvement of protein kinase C- and nuclear factor-κB-dependent mechanisms. / Kuo, Chen Tzu; Chiang, Ling Ling; Lee, Chun-Nin; Yu, Ming Chih; Bai, Kuan Jen; Lee, Horng Mo; Lee, Wen Sen; Sheu, Joen Rong; Lin, Chien Huang.

於: Journal of Biomedical Science, 卷 10, 編號 1, 2003, p. 136-145.

研究成果: 雜誌貢獻 › 文章

Kuo, CT, Chiang, LL, Lee, C-N, Yu, MC, Bai, KJ, Lee, HM, Lee, WS, Sheu, JR & Lin, CH 2003, 'Induction of nitric oxide synthase in RAW 264.7 macrophages by lipoteichoic acid from Staphylococcus aureus: Involvement of protein kinase C- and nuclear factor-κB-dependent mechanisms', Journal of Biomedical Science, 卷 10, 編號 1, 頁 136-145. https://doi.org/10.1159/000068076
Kuo CT, Chiang LL, Lee C-N, Yu MC, Bai KJ, Lee HM 等. Induction of nitric oxide synthase in RAW 264.7 macrophages by lipoteichoic acid from Staphylococcus aureus: Involvement of protein kinase C- and nuclear factor-κB-dependent mechanisms. Journal of Biomedical Science. 2003;10(1):136-145. https://doi.org/10.1159/000068076
Kuo, Chen Tzu ; Chiang, Ling Ling ; Lee, Chun-Nin ; Yu, Ming Chih ; Bai, Kuan Jen ; Lee, Horng Mo ; Lee, Wen Sen ; Sheu, Joen Rong ; Lin, Chien Huang. / Induction of nitric oxide synthase in RAW 264.7 macrophages by lipoteichoic acid from Staphylococcus aureus : Involvement of protein kinase C- and nuclear factor-κB-dependent mechanisms. 於: Journal of Biomedical Science. 2003 ; 卷 10, 編號 1. 頁 136-145.
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abstract = "This study investigates the signaling pathway involved in inducible nitric oxide synthase (iNOS) expression and nitric oxide (NO) release caused by Staphylococcus aureus lipoteichoic acid (LTA) in RAW 264.7 macrophages. A phosphatidylcholine-phospholipase C (PC-PLC) inhibitor (D-609) and a phosphatidylinositol-phospholipase C (PI-PLC) inhibitor (U-73122) attenuated LTA-induced iNOS expression and NO release. Two PKC inhibitors (Go 6976 and Ro 31-8220), an NF-κB inhibitor (pyrrolidine dithiocarbamate; PDTC), and long-term (24 h) 12-phorbol-13-myristate acetate (PMA) treatment each also inhibited LTA-induced iNOS expression and NO release. Treatment of cells with LTA caused an increase in PKC activity; this stimulatory effect was inhibited by D-609, U-73122, or Ro 31-8220. Stimulation of cells with LTA caused IκB-α phosphorylation and IκB-α degradation in the cytosol, and translocation of p65 and p50 NF-κB from the cytosol to the nucleus. Treatment of cells with LTA caused NF-κB activation by detecting the formation of NF-κB-specific DNA-protein complexes in the nucleus; this effect was inhibited by Go 6976, Ro 31-8220, long-term PMA treatment, PDTC, L-1-tosylamido-2-phenylethyl chloromethyl ketone (TPCK), and calpain inhibitor I. These results suggest that LTA might activate PC-PLC and PI-PLC to induce PKC activation, which in turn initiates NF-κB activation, and finally induces iNOS expression and NO release in RAW 264.7 macrophages.",
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AU - Kuo, Chen Tzu

AU - Chiang, Ling Ling

AU - Lee, Chun-Nin

AU - Yu, Ming Chih

AU - Bai, Kuan Jen

AU - Lee, Horng Mo

AU - Lee, Wen Sen

AU - Sheu, Joen Rong

AU - Lin, Chien Huang

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N2 - This study investigates the signaling pathway involved in inducible nitric oxide synthase (iNOS) expression and nitric oxide (NO) release caused by Staphylococcus aureus lipoteichoic acid (LTA) in RAW 264.7 macrophages. A phosphatidylcholine-phospholipase C (PC-PLC) inhibitor (D-609) and a phosphatidylinositol-phospholipase C (PI-PLC) inhibitor (U-73122) attenuated LTA-induced iNOS expression and NO release. Two PKC inhibitors (Go 6976 and Ro 31-8220), an NF-κB inhibitor (pyrrolidine dithiocarbamate; PDTC), and long-term (24 h) 12-phorbol-13-myristate acetate (PMA) treatment each also inhibited LTA-induced iNOS expression and NO release. Treatment of cells with LTA caused an increase in PKC activity; this stimulatory effect was inhibited by D-609, U-73122, or Ro 31-8220. Stimulation of cells with LTA caused IκB-α phosphorylation and IκB-α degradation in the cytosol, and translocation of p65 and p50 NF-κB from the cytosol to the nucleus. Treatment of cells with LTA caused NF-κB activation by detecting the formation of NF-κB-specific DNA-protein complexes in the nucleus; this effect was inhibited by Go 6976, Ro 31-8220, long-term PMA treatment, PDTC, L-1-tosylamido-2-phenylethyl chloromethyl ketone (TPCK), and calpain inhibitor I. These results suggest that LTA might activate PC-PLC and PI-PLC to induce PKC activation, which in turn initiates NF-κB activation, and finally induces iNOS expression and NO release in RAW 264.7 macrophages.

AB - This study investigates the signaling pathway involved in inducible nitric oxide synthase (iNOS) expression and nitric oxide (NO) release caused by Staphylococcus aureus lipoteichoic acid (LTA) in RAW 264.7 macrophages. A phosphatidylcholine-phospholipase C (PC-PLC) inhibitor (D-609) and a phosphatidylinositol-phospholipase C (PI-PLC) inhibitor (U-73122) attenuated LTA-induced iNOS expression and NO release. Two PKC inhibitors (Go 6976 and Ro 31-8220), an NF-κB inhibitor (pyrrolidine dithiocarbamate; PDTC), and long-term (24 h) 12-phorbol-13-myristate acetate (PMA) treatment each also inhibited LTA-induced iNOS expression and NO release. Treatment of cells with LTA caused an increase in PKC activity; this stimulatory effect was inhibited by D-609, U-73122, or Ro 31-8220. Stimulation of cells with LTA caused IκB-α phosphorylation and IκB-α degradation in the cytosol, and translocation of p65 and p50 NF-κB from the cytosol to the nucleus. Treatment of cells with LTA caused NF-κB activation by detecting the formation of NF-κB-specific DNA-protein complexes in the nucleus; this effect was inhibited by Go 6976, Ro 31-8220, long-term PMA treatment, PDTC, L-1-tosylamido-2-phenylethyl chloromethyl ketone (TPCK), and calpain inhibitor I. These results suggest that LTA might activate PC-PLC and PI-PLC to induce PKC activation, which in turn initiates NF-κB activation, and finally induces iNOS expression and NO release in RAW 264.7 macrophages.

KW - Inducible nitric oxide synthase

KW - Lipoteichoic acid

KW - NF-κB

KW - Nitric oxide

KW - Protein kinase C

KW - RAW 264.7 macrophages

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