Lipopolysaccharide induces autotaxin expression in human monocytic THP-1 cells

Li, Song; Zhang, Junjie

doi:10.1016/j.bbrc.2008.11.047

Cited by 34 publications

(36 citation statements)

References 25 publications

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“…LPS stimulation of monocytes/macrophages effects the generation of a number of inflammatory mediators. We have previously demonstrated that LPS induces ATX expression in human monocytic THP-1 cell and that the activation of PKR, JNK and p38 MAPK is required for the ATX induction [14]. In this study, it is found that LPS induces both ATX and LPA 3 expression in human monocytic THP-1 cells.…”

Section: Introductionsupporting

confidence: 52%

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ATX and LPA receptor 3 are coordinately up‐regulated in lipopolysaccharide‐stimulated THP‐1 cells through PKR and SPK1‐mediated pathways

2012

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Edited by Beat Imhof Keywords:Lysophosphatidic acid Autotaxin LPA receptor 3 Lipopolysaccharide THP-1 cell CCL8 a b s t r a c t Lysophosphatidic acid (LPA) is an important phospholipid mediator in inflammation and immunity. Previously, we showed that autotaxin (ATX), the enzyme producing LPA from lysophosphatidylcholine (LPC), is induced by LPS in THP-1 cells via the activation of PKR, JNK and p38 MAPK. In this study, we find that ATX and LPA receptor 3 (LPA 3 ) are coordinately up-regulated in LPS-stimulated THP-1 cells. PKR-mediated activation of JNK1 and p38 MAPK is required for both ATX and LPA 3 up-regulation. SPK1-mediated activation of the PI3K-AKT-b-catenin pathway is essential for ATX induction, while SPK1-mediated ERK activation is required for LPA 3 up-regulation. Either ATX or LPA 3 knockdown inhibited CCL8 induction by LPS, suggesting that ATX and LPA 3 are involved in CCL8 induction during the inflammatory process against bacterial infection.

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Section: Introductionsupporting

confidence: 52%

“…We had reported that LPS induced ATX expression in monocytic THP-1 cells, which was suppressed when PKR, JNK or p38 MAPK activation was inhibited by its specific inhibitor [14]. In present study, PKR, p38 and JNK1/2 were downregulated with their specific siRNA, respectively.…”

Section: Pkr-mediated Activation Of Jnk1 and P38 Mapk Is Required Forsupporting

confidence: 43%

ATX and LPA receptor 3 are coordinately up‐regulated in lipopolysaccharide‐stimulated THP‐1 cells through PKR and SPK1‐mediated pathways

2012

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“…Briefly, antigen retrieval was performed in 0.01 M citrate buffer (pH 6.0), followed by quenching of endogenous peroxidase activity with 3% H 2 O 2 in methanol. Sections were then incubated with MMP-9 (Abcam, Cambridge, UK) and ATX (as described Li and Zhang, 2009) primary antibodies overnight at 4°C. Powervision horseradish peroxidase-IgG was used as secondary antibody.…”

Section: Methodsmentioning

confidence: 99%

Lysophosphatidic Acid Is Associated with Atherosclerotic Plaque Instability by Regulating NF-κB Dependent Matrix Metalloproteinase-9 Expression via LPA2 in Macrophages

Wang

Zhao

et al. 2017

Front. Physiol.

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Lysophosphatidic acid (LPA), one of the simplest phospholipid signaling molecules, participates in formation and disruption of atherosclerotic plaque. Matrix metalloproteinases (MMPs) contribute to atherosclerotic plaque rupture by involving in extracellular matrix (ECM) degradation and then thinning fibrous cap. Our previous study demonstrated that macrophage-derived MMP-9 was associated with coronary plaque instability, but the relationship between LPA and MMP-9 remains unclear. The present work therefore aimed at elucidating association between LPA and MMP-9 and the regulation mechanism of LPA on MMP-9 in macrophages. We found that plasma LPA and MMP-9 levels were correlated positively (r = 0.31, P < 0.05) and both elevated significantly in patients with acute myocardial infarct (AMI). Consistent with peripheral blood levels, histochemical staining indicated that autotaxin (ATX), LPA-producing ectoenzyme, and MMP-9 were expressed frequently in the necrotic core and fibrous cap of human unstable plaques, which might increase the instability of plaque. Experiments in vitro were done with THP-1-derived macrophages and showed that LPA enhanced the expression, secretion and activity of MMP-9 in a time- and dose-dependent manner. Induction of LPA on pro-MMP-9 and active-MMP-9 was confirmed in human peripheral blood monocyte-derived macrophages. PDTC, NF-κB inhibitor, but not inhibitor of AP-1 and PPARγ, effectively prevented LPA-induced MMP-9 expression and NF-κB p65 siRNA decreased MMP-9 transcription, confirming that LPA might induce MMP-9 elevation by activating NF-κB pathway. In addition, knockdown of LPA2 attenuated LPA-induced MMP-9 expression and nucleus p65 levels. These findings revealed that LPA upregulated the expression of MMP-9 through activating NF-κB pathway in the LPA2 dependent manner, hence blocking LPA receptors signaling may provide therapeutic strategy to target plaque destabilization.

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“…However, whether ENPP2 can affect replication of hepatitis B virus remained unknown. Recognized as an enzyme secreted by the liver, ENPP2 exerts lysophospholipase D (lysoPLD) activity for generating lysophosphatidic acid (LPA) from lysophosphatidylcholine (LPC) [31]. Moreover, ENPP2 seems to be the predominant enzyme-generating LPA in plasma and serum [32, 33].…”

Section: Discussionmentioning

confidence: 99%

Proteomics Based Identification of Autotaxin As An Anti-Hepatitis B Virus Factor and a Promoter of Hepatoma Cell Invasion and Migration

She¹,

Yang²,

Hu³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Hepatitis B virus (HBV) infection is a major cause of cirrhosis and hepatocellular carcinoma. Therefore, we aimed to obtain further information on HBV pathogenesis, and to search for novel putative molecules for anti-HBV therapy. Methods: We utilized Isobaric Tags for Relative and Absolute Quantitation (iTRAQ) to identify the secretory proteins that are differentially expressed in the HBV DNA-transfected HepG2.2.15 cell line and its parental HepG2 cell line. Immunohistochemistry (IHC) was employed to assess the clinical relevance of the observations. Small interfering (si)RNA-based silencing transfection methods were carried out to study the function of ENPP2. Results: Totally, 133 unique proteins were identified as differentially expressed in HepG2.2.15 cell line compared with HepG2 cell line. Ectonucleotide pyrophosphatase/phosphodiesterase family member 2 precursor (ENPP2) is one of the most significantly up-regulated secretory proteins associated with HBV replication. This differential expression of ENPP2 was further validated by real-time quantitative RT-PCR, Western Blot and immunohistochemical analysis. To study the function of ENPP2, we knockdown ENPP2 expression in HepG2.2.15 cell line by RNA interference. ENPP2 silencing increased HBV replication approximately 2.3-fold by enhancing, via the type I IFN signaling pathway, HBV cccDNA (covalently closed circular DNA) translation into viral RNA. Moreover, attenuation of ENPP2 expression inhibited both the invasion and migration ability of hepatoma cells in vitro via interacting with the molecules in the tumor microenvironment. Conclusion: Our study demonstrates that ENPP2 may be a novel anti-HBV target and indicate that suppression of its expression may inhibit the invasion and migration ability of hepatoma cells.

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Lipopolysaccharide induces autotaxin expression in human monocytic THP-1 cells

Cited by 34 publications

References 25 publications

ATX and LPA receptor 3 are coordinately up‐regulated in lipopolysaccharide‐stimulated THP‐1 cells through PKR and SPK1‐mediated pathways

ATX and LPA receptor 3 are coordinately up‐regulated in lipopolysaccharide‐stimulated THP‐1 cells through PKR and SPK1‐mediated pathways

Lysophosphatidic Acid Is Associated with Atherosclerotic Plaque Instability by Regulating NF-κB Dependent Matrix Metalloproteinase-9 Expression via LPA2 in Macrophages

Proteomics Based Identification of Autotaxin As An Anti-Hepatitis B Virus Factor and a Promoter of Hepatoma Cell Invasion and Migration

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