Epigallocatechin-3-Gallate Inhibits Matrix Metalloproteinase-9 and Monocyte Chemotactic Protein-1 Expression Through the 67-κDa Laminin Receptor and the TLR4/MAPK/NF-κB Signalling Pathway in Lipopolysaccharide-Induced Macrophages

Li, Yafei; Wang, Hao; Fan, Yi; Shi, Haojie; Wang, Qiming; Chen, Bingrui; Khurwolah, Mohammad Reeaze; Long, Qingqing; Wang, Si-Bo; Wang, Ze‐Mu; Wang, Liansheng

doi:10.1159/000481643

Cited by 39 publications

(23 citation statements)

References 28 publications

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“…These findings suggest that LPS induces brain inflammation via induction of MMP-9 expression, leading to an increase of BBB permeability, recruitment of immune cells, cell migration, and tissue remodeling during brain insults [8]. The effects of LPS on cells are mediated by a family of TLRs on various types of cells [18,20]. Among these TLRs, TLR4 is activated by LPS [24].…”

Section: Discussionmentioning

confidence: 99%

“…The effects of LPS on cells are mediated by a family of TLRs on various types of cells [18,20]. Among these TLRs, TLR4 is activated by LPS [24].…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies have shown that LPS can activate several downstream signaling molecules of TLR4, such as proto-oncogene tyrosine-protein kinase (c-Src) [18], proline-rich tyrosine kinase 2 (Pyk2) [19], platelet-derived growth factor receptor (PDGFR)/phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) [18], and mitogen-activated protein kinases (MAPKs) [20] to trigger activator protein 1 (AP-1) activity [17] and enhance the expression of inflammatory proteins, including MMP-9, monocyte chemotactic protein-1, IL-8, and intercellular adhesion molecule-1 (ICAM-1), in various types of cells. LPS can also induce MMP-9 expression in macrophages and animals [20,21]. However, in rat brain astrocytes (RBA-1) cells, the detailed mechanisms underlying MMP-9 expression induced by LPS is not well understood.In the present study, we dissected the signaling component-linked AP-1 activation to MMP-9 expression induced by LPS in RBA-1 cells.…”

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confidence: 99%

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Lipopolysaccharide-Induced Matrix Metalloproteinase-9 Expression Associated with Cell Migration in Rat Brain Astrocytes

Yang

Lin

Hsiao

et al. 2019

IJMS

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Neuroinflammation is a landmark of neuroinflammatory and neurodegenerative diseases. Matrix metalloproteinase (MMP)-9, one member of MMPs, has been shown to contribute to the pathology of these brain diseases. Several experimental models have demonstrated that lipopolysaccharide (LPS) exerts a pathological role through Toll-like receptors (TLRs) in neuroinflammation and neurodegeneration. However, the mechanisms underlying LPS-induced MMP-9 expression in rat brain astrocytes (RBA-1) are not completely understood. Here, we applied pharmacological inhibitors and siRNA transfection to assess the levels of MMP-9 protein, mRNA, and promoter activity, as well as protein kinase phosphorylation in RBA-1 cells triggered by LPS. We found that LPS-induced expression of pro-form MMP-9 and cell migration were mediated through TLR4, proto-oncogene tyrosine-protein kinase (c-Src), proline-rich tyrosine kinase 2 (Pyk2), platelet-derived growth factor receptor (PDGFR), phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt), p38 mitogen-activated protein kinase (MAPK), and Jun amino-terminal kinase (JNK)1/2 signaling molecules in RBA-1 cells. In addition, LPS-stimulated binding of c-Jun to the MMP-9 promoter was confirmed by chromatin immunoprecipitation (ChIP) assay, which was blocked by pretreatment with c-Src inhibitor II, PF431396, AG1296, LY294002, Akt inhibitor VIII, p38 MAP kinase inhibitor VIII, SP600125, and tanshinone IIA. These results suggest that in RBA-1 cells, LPS activates a TLR4/c-Src/Pyk2/PDGFR/PI3K/Akt/p38 MAPK and JNK1/2 pathway, which in turn triggers activator protein 1 (AP-1) activation and ultimately induces MMP-9 expression and cell migration.

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Section: Discussionmentioning

confidence: 99%

“…The effects of LPS on cells are mediated by a family of TLRs on various types of cells [18,20]. Among these TLRs, TLR4 is activated by LPS [24].…”

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Lipopolysaccharide-Induced Matrix Metalloproteinase-9 Expression Associated with Cell Migration in Rat Brain Astrocytes

Yang

Lin

Hsiao

et al. 2019

IJMS

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“…In addition, many studies showed that EGCG specifically inhibits the inflammatory mediators and cytokine levels through the 67-kDa laminin receptor (67LR) as a cell-surface EGCG receptor in LPS-stimulated various cells, such as adipocytes, macrophage, and cerebral microvascular endothelial cells [11-13]. Furthermore, 67LR signaling can activate TLR negative regulator, the Toll-interacting protein (Tollip), in macrophages [12]. However, the precise mechanisms for inhibition of excessive inflammatory response induced by EGCG treatment in IBD patients still remain largely unknown.…”

Section: Introductionmentioning

confidence: 99%

Epigallocatechin-3-Gallate Regulates Anti-Inflammatory Action Through 67-kDa Laminin Receptor-Mediated Tollip Signaling Induction in Lipopolysaccharide-Stimulated Human Intestinal Epithelial Cells

Byun

Kim

Sung

et al. 2018

Cell Physiol Biochem

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Background/Aims: Inflammatory bowel disease (IBD) is a condition that involves chronic inflammation in all or part of the digestive tract. Often painful and debilitating, IBD can lead to life-threatening complications and increase the risk for colon cancer. In this study, we investigated the epigallocatechin-3-gallate (EGCG) mediated anti-inflammation response in lipopolysaccharide (LPS)-stimulated human colorectal cells through the negative regulator of Toll-like receptor (TLR) signaling. Methods: human intestinal epithelial cells (HT-29) were used in all experiments. Cell cytotoxicity and nitric oxide (NO) were evaluated by WST-1 and the Griess reagent. Western blot analysis and ELISA were used to determine inflammatory mediators and 67-kDa laminin receptor (67LR)-mediated Tollip signaling pathways. Results: Treatment of EGCG and LPS did not affect the cytotoxicity in HT-29 cells. LPS treatment dose-dependently increased the pro-inflammatory cytokine, such as interleukin (IL)-8, whereas EGCG significantly reduced the LPS-stimulated IL-8 production. Additionally, EGCG treatment markedly increased the Toll-interacting protein (Tollip) expression, which negatively regulates the TLR signaling in a dose and time-dependent manner. In particular, in the result from an RNA interference-mediated assay, our finding showed that silencing of Tollip resulted in abrogation of the inhibitory action of EGCG on LPS-induced production of pro-inflammatory mediators (inducible nitric oxide synthase-mediated NO/COX2, and IL-8) and activation of MAPKs and NF-κB signaling pathways. Interestingly, we also found that Tollip expression induced by EGCG could be modulated through 67LR expressed on the surface of HT-29 cells. Conclusions: Our novel finding indicates that 67LR and Tollip signaling activated by EGCG treatment is essential for inhibition of inflammation in human intestinal epithelial cells.

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“…Among green tea polyphenols, known as flavanoids or catechins, the epigallocatechin-3-gallate (EGCG) is the main molecular component known to exert many biological effects [1][2][3][4][5][6][7][8].…”

Section: Introductionmentioning

confidence: 99%

Long-Term Oral Administration of Theaphenon-E Improves Cardiomyocyte Mechanics and Calcium Dynamics by Affecting Phospholamban Phosphorylation and ATP Production

Bocchi

Savi

Naponelli

et al. 2018

Cell Physiol Biochem

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Background/Aims: Dietary polyphenols from green tea have been shown to possess cardio-protective activities in different experimental models of heart diseases and age-related ventricular dysfunction. The present study was aimed at evaluating whether long term in vivo administration of green tea extracts (GTE), can exert positive effects on the normal heart, with focus on the underlying mechanisms. Methods: The study population consisted of 20 male adult Wistar rats. Ten animals were given 40 mL/day tap water solution of GTE (concentration 0.3%) for 4 weeks (GTE group). The same volume of water was administered to the 10 remaining control rats (CTRL). Then, in vivo and ex vivo measurements of cardiac function were performed in the same animal, at the organ (hemodynamics) and cellular (cardiomyocyte mechanical properties and intracellular calcium dynamics) levels. On cardiomyocytes and myocardial tissue samples collected from the same in vivo studied animals, we evaluated: (1) the intracellular content of ATP, (2) the endogenous mitochondrial respiration, (3) the expression levels of the Sarcoplasmic Reticulum Ca²⁺-dependent ATPase 2a (SERCA2), the Phospholamban (PLB) and the phosphorylated form of PLB, the L-type Ca²⁺ channel, the Na⁺-Ca²⁺ exchanger, and the ryanodine receptor 2. Results: GTE cardiomyocytes exhibited a hyperdynamic contractility compared with CTRL (the rate of shortening and re-lengthening, the fraction of shortening, the amplitude of calcium transient, and the rate of cytosolic calcium removal were significantly increased). A faster isovolumic relaxation was also observed at the organ level. Consistent with functional data, we measured a significant increase in the intracellular ATP content supported by enhanced endogenous mitochondrial respiration in GTE cardiomyocytes, as well as higher values of the ratios phosphorylated-PLB/PLB and SERCA2/PLB. Conclusions: Long-term in vivo administration of GTE improves cell mechanical properties and intracellular calcium dynamics in normal cardiomyocytes, by increasing energy availability and removing the inhibitory effect of PLB on SERCA2.

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Epigallocatechin-3-Gallate Inhibits Matrix Metalloproteinase-9 and Monocyte Chemotactic Protein-1 Expression Through the 67-κDa Laminin Receptor and the TLR4/MAPK/NF-κB Signalling Pathway in Lipopolysaccharide-Induced Macrophages

Cited by 39 publications

References 28 publications

Lipopolysaccharide-Induced Matrix Metalloproteinase-9 Expression Associated with Cell Migration in Rat Brain Astrocytes

Lipopolysaccharide-Induced Matrix Metalloproteinase-9 Expression Associated with Cell Migration in Rat Brain Astrocytes

Epigallocatechin-3-Gallate Regulates Anti-Inflammatory Action Through 67-kDa Laminin Receptor-Mediated Tollip Signaling Induction in Lipopolysaccharide-Stimulated Human Intestinal Epithelial Cells

Long-Term Oral Administration of Theaphenon-E Improves Cardiomyocyte Mechanics and Calcium Dynamics by Affecting Phospholamban Phosphorylation and ATP Production

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