MAP Kinase activation is required for the MMP-9 induction by TNF-stimulation

Kim, Kyung Chan; Lee, Chu Hee

doi:10.1007/bf02978209

Cited by 34 publications

(23 citation statements)

References 24 publications

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“…ERK1/2, JNK, and p38 MAPK) in the production of MMP-9 in response to TNF-␣ appears to be cell-specific. For example, ERK1/2 but not JNK or p38 MAPK was found to be involved in TNF-␣-induced MMP-9 expression in a human monocyte cell line (53). In human trophoblastic cells, TNF-␣-induced MMP-9 expression, secretion, and activity were completely blocked by JNK and ERK1/2 inhibitors but not by p38 MAPK inhibitors (54).…”

Section: Discussionmentioning

confidence: 94%

Tumor Necrosis Factor-α Augments Matrix Metalloproteinase-9 Production in Skeletal Muscle Cells through the Activation of Transforming Growth Factor-β-activated Kinase 1 (TAK1)-dependent Signaling Pathway

Srivastava

Qin

Wedhas

et al. 2007

Journal of Biological Chemistry

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Section: Discussionmentioning

confidence: 94%

Tumor Necrosis Factor-α Augments Matrix Metalloproteinase-9 Production in Skeletal Muscle Cells through the Activation of Transforming Growth Factor-β-activated Kinase 1 (TAK1)-dependent Signaling Pathway

Srivastava

Qin

Wedhas

et al. 2007

Journal of Biological Chemistry

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“…Several studies have indicated that MAPK pathways are involved in the expression of MMP-9 (33,34). To explore whether the inhibitory effect of aspirin on the expression of MMP-9 was mediated through the MAPK pathway, the phosphorylated protein levels of ERK1/2, JNK and p38 were examined by western blot in RAW264.7 cells pre-treated with aspirin and then with TNF-α for various times (0, 10, 20, 30 and 60 min).…”

Section: Effect Of Aspirin On the Inhibition Of Erk1/2 Jnk And P38mentioning

confidence: 99%

Aspirin suppresses TNF‑α‑induced MMP‑9 expression via NF‑κB and MAPK signaling pathways in RAW264.7 cells

Zhang

Huang

et al. 2017

Exp Ther Med

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Abstract. Numerous studies have indicated that the expression of matrix metalloproteinase-9 (MMP-9) contributes to the atherosclerotic plaque hemorrhage and rupture. Aspirin, a non-steroidal anti-inflammation drug, has been known for its anti-platelet effect in the prevention of the vascular complications of atherosclerosis. The present study aimed to investigate the pharmacological effects of aspirin on tumor necrosis factor-α (TNF-α)-induced MMP-9 expression and the underlying molecular mechanisms in murine macrophage RAW264.7 cells. Western blot analysis indicated that the protein level of MMP-9 was reduced by aspirin in a dose-dependent manner. In addition, downregulation of MMP-9 mRNA and activity were detected in aspirin-treated cells using quantitative polymerase chain reaction and a gelatin zymography assay separately. It was also observed that aspirin has a suppressive effect on the activation of nuclear factor (NF)-κB and inhibits the phosphorylation of mitogen-activated protein kinases (MAPKs), including extracellular signal-regulated kinases 1/2, p38 and c-Jun N-terminal kinase. Furthermore, subsequent to inhibition of the MAPK pathway by specific inhibitors (PD98059, SB203580 and SP600125), the expression of MMP-9 was reduced, indicating that the inhibitory effect of aspirin on MMP-9 in TNF-α-treated RAW264.7 cells may be, at least in part, through suppression of NF-κB activation and the MAPK pathway. These findings support the notion that aspirin has therapeutic potential application in the prevention and treatment of atherosclerosis disease.

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“…Many of these signals are generated during the LPS response or during infection. For instance, interleukin-1␤ (IL-1␤) and TNF, both of which are important cytokines in endotoxemia and sepsis, can induce MMP genes (60,129). In turn, MMPs can activate these cytokines and/or release them by shedding, generating a positive feedback loop.…”

Section: Different Cell Types Can Produce Mmps In Response To Lps Sumentioning

confidence: 99%

Matrix Metalloproteinases as Drug Targets in Infections Caused by Gram-Negative Bacteria and in Septic Shock

2009

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SUMMARY The mammalian immune system is optimized to cope effectively with the constant threat of pathogens. However, when the immune system overreacts, sepsis, severe sepsis, or septic shock can develop. Despite extensive research, these conditions remain the leading cause of death in intensive care units. The matrix metalloproteinases (MMPs) constitute a family of proteases that are expressed in developmental, physiological, and pathological processes and also in response to infections. Studies using MMP inhibitors and MMP knockout mice indicate that MMPs play essential roles in infection and in the host defense against infection. This review provides a brief introduction to some basic concepts of infections caused by gram-negative bacteria and reviews reports describing MMP expression and inhibition, as well as studies with MMP-deficient mice in models of infection caused by gram-negative bacteria and of septic shock. We discuss whether MMPs should be considered novel drug targets in infection and septic shock.

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MAP Kinase activation is required for the MMP-9 induction by TNF-stimulation

Cited by 34 publications

References 24 publications

Tumor Necrosis Factor-α Augments Matrix Metalloproteinase-9 Production in Skeletal Muscle Cells through the Activation of Transforming Growth Factor-β-activated Kinase 1 (TAK1)-dependent Signaling Pathway

Tumor Necrosis Factor-α Augments Matrix Metalloproteinase-9 Production in Skeletal Muscle Cells through the Activation of Transforming Growth Factor-β-activated Kinase 1 (TAK1)-dependent Signaling Pathway

Aspirin suppresses TNF‑α‑induced MMP‑9 expression via NF‑κB and MAPK signaling pathways in RAW264.7 cells

Matrix Metalloproteinases as Drug Targets in Infections Caused by Gram-Negative Bacteria and in Septic Shock

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