Interleukin-6 Released from Fibroblasts Is Essential for Up-regulation of Matrix Metalloproteinase-1 Expression by U937 Macrophages in Coculture

Sundararaj, Kamala; Samuvel, Devadoss J.; Li, Yanchun; Sanders, John J.; Lopes‐Virella, Maria F.; Huang, Yan

doi:10.1074/jbc.m806573200

Cited by 86 publications

(71 citation statements)

References 34 publications

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“…The up-regulation of MMP-1 protein expression followed by inhibition of its activity after exposure to Si/SiO 2 QDs could be explained by the elevated level of TIMP-1 expression, an endogenous inhibitor of this enzyme [53]. Additionally, the release of IL-6 might be responsible for the upregulation of MMP-1 expression as reported previously [54]. These changes in MMPs expression and activity were similar to the molecular events involved in the pathogenesis of chronic rhino-sinusitis without nasal polyps, which involves high levels of IL-6 and IL-8 that trigger fibrosis by up-regulating TIMP-1 in fibroblasts [55].…”

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confidence: 62%

Silicon‐based quantum dots induce inflammation in human lung cells and disrupt extracellular matrix homeostasis

et al. 2015

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Quantum dots (QDs) are nanocrystalline semiconductor materials that have been tested for biological applications such as cancer therapy, cellular imaging and drug delivery, despite the serious lack of information of their effects on mammalian cells. The present study aimed to evaluate the potential of Si/SiO 2 QDs to induce an inflammatory response in MRC-5 human lung fibroblasts. Cells were exposed to different concentrations of Si/SiO 2 QDs (25-200 lgÁmL À1 ) for 24, 48, 72 and 96 h. The results obtained showed that uptake of QDs was dependent on biocorona formation and the stability of nanoparticles in various biological media (minimum essential medium without or with 10% fetal bovine serum). The cell membrane damage indicated by the increase in lactate dehydrogenase release after exposure to QDs was dose-and time-dependent. The level of lysosomes increased proportionally with the concentration of QDs, whereas an accumulation of autophagosomes was also observed. Cellular morphology was affected, as shown by the disruption of actin filaments. The enhanced release of nitric oxide and the increase in interleukin-6 and interleukin-8 protein expression suggested that nanoparticles triggered an inflammatory response in MRC-5 cells. QDs decreased the protein expression and enzymatic activity of matrix metalloproteinase (MMP)-2 and MMP-9 and also MMP-1 caseinase activity, whereas the protein levels of MMP-1 and tissue inhibitor of metalloproteinase-1 increased. The present study reveals for the first time that silicon-based QDs are able to generate inflammation in lung cells and cause an imbalance in extracellular matrix turnover through a differential regulation of MMPs and tissue inhibitor of metalloproteinase-1 protein expression.

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confidence: 62%

Silicon‐based quantum dots induce inflammation in human lung cells and disrupt extracellular matrix homeostasis

et al. 2015

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“…The medium was changed every 2–3 days. Our previous studies have shown the similarity between U937 cells and human monocytes in cellular response to LPS (Samuvel et al; Sundararaj et al, 2008; Sundararaj et al, 2009). For cell treatment, LPS from E. coli (Ec) (Sigma, St. Louis, MO) and pam2CSK4 and pam3CSK4 (InvivoGen, San Diego, CA) were used.…”

Section: Methodsmentioning

confidence: 87%

Coactivation of TLR4 and TLR2/6 coordinates an additive augmentation on IL-6 gene transcription via p38MAPK pathway in U937 mononuclear cells

Jin

Samuvel

Zhang

et al. 2011

Molecular Immunology

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Studies have demonstrated that TLR4 and TLR2 expression by monocytes and the blood levels of TLR4 and TLR2 ligand in diabetic patients are significantly incased compared to nondiabetic patients, indicating that more monocytes in diabetic patients may have coactivation of TLR4 and TLR2. Although it has been shown that either TLR4 or TLR2 activation leads to increased expression of proinflammatory cytokines, the effect of coactivation of TLR2 and TLR4 in mononuclear cells on proinflammatory cytokine expression and the underlying molecular mechanisms remain largely unknown. In this study, we found that while TLR1, TLR2, TLR4 and TLR6 were expressed by U937 mononuclear cells, TLR4 was expressed at the highest level. Interestingly, results showed that while activation of either TLR4 or TLR2/6 (TLR2 dimerized with TLR6), but not TLR2/1 (TLR2 dimerized with TLR1), significantly increased IL-6 expression by U937 mononuclear cells, coactivation of TLR4 and TLR2/6, but not TLR4 and TLR2/1, led to a further augmentation on IL-6 expression by increasing IL-6 transcriptional activity, but not mRNA stability. To explore the signaling mechanisms involved in the augmentation, we found that p38 MAPK and NFκB pathways, but not ERK and JNK pathways, were required for the augmentation of IL-6 expression by coactivation of TLR4 and TLR2/6. Furthermore, we found that coactivation of TLR4 and TLR2/6 increased p38 phosphorylation, but not NFkB activity, as compared to activation of TLR4 or TLR2/6 alone. Taken together, this study showed that coactivation of TLR4 and TLR2/6 coordinates an additive augmentation of IL-6 gene transcription via p38 MAPK pathway in U937 mononuclear cells.

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“…Carlsbad, CA) containing normal glucose (5 mM) or high glucose (25 mM), 10% fetal calf serum, 1% MEM non-essential amino acid solution, and 0.6 g/100 ml of HEPES. Five and 25 mM of glucose have been used commonly as the concentrations of normal and high glucose, respectively (Nareika et al, 2008, Nareika et al, 2007, Sundararaj et al, 2009). …”

Section: Methodsmentioning

confidence: 99%

Matrix metalloproteinase‐8 expression in periodontal tissues surgically removed from diabetic and non‐diabetic patients with periodontal disease

Hardy

Ross

Schuyler

et al. 2011

J Clinic Periodontology

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Background Although it is known that periodontal MMP-8 expression is associated with periodontal disease, the information concerning the periodontal MMP-8 expression in diabetic patients with periodontal disease is insufficient. Materials and Methods Periodontal tissue specimens were collected from 7 patients without periodontal disease and diabetes (Group 1), 15 patients with periodontal disease alone (Group 2) and 10 patients with both periodontal disease and diabetes (Group 3). The frozen sections were prepared and MMP-8 protein expression was detected using immunohistochemistry and quantified. For in vitro study, human U937 mononuclear cells were pre-exposed to normal or high glucose and then treated with LPS. Results The nonparametric Kruskal-Wallis test showed that the difference in MMP-8 protein levels among the three groups were statistically significant (p = 0.003). Nonparametric analysis using Jonckheere-Terpstra test showed a tendency of increase in periodontal MMP-8 levels across Group 1 to Group 2 to Group 3 (p = 0.0002). In vitro studies showed that high glucose and LPS had a synergistic effect on MMP-8 expression. Conclusion Our current study showed an increasing trend in MMP-8 protein expression levels across patients without both periodontal disease and diabetes, patients with periodontal disease alone and patients with both diseases.

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Interleukin-6 Released from Fibroblasts Is Essential for Up-regulation of Matrix Metalloproteinase-1 Expression by U937 Macrophages in Coculture

Cited by 86 publications

References 34 publications

Silicon‐based quantum dots induce inflammation in human lung cells and disrupt extracellular matrix homeostasis

Silicon‐based quantum dots induce inflammation in human lung cells and disrupt extracellular matrix homeostasis

Coactivation of TLR4 and TLR2/6 coordinates an additive augmentation on IL-6 gene transcription via p38MAPK pathway in U937 mononuclear cells

Matrix metalloproteinase‐8 expression in periodontal tissues surgically removed from diabetic and non‐diabetic patients with periodontal disease

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