NF-κB Mediated IL-6 Production by Renal Epithelial Cells Is Regulated by C-Jun NH2-Terminal Kinase

Haij, Simone de; Bakker, Astrid C.; Geest, Reinier N. van der; Haegeman, Guy; Berghe, Wim Vanden; Aarbiou, Jamil; Daha, Mohamed R.; Kooten, Cees van

doi:10.1681/asn.2004090781

Cited by 52 publications

(36 citation statements)

References 46 publications

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“…In this sense, MCP-1 overexpression is regulated by all three MAPKs, as described for other factors involved in renal inflammation, such as angiotensin II. 47 We observed that JNK activation by CTGF also regulates IL-6 overexpression, as observed in human tubuloepithelial cells in response to IL-1␤ 48 . In vivo p38 inhibition reduced renal MCP-1 levels and the severity of tissue injury but did not suppress renal levels of IL-6.…”

Section: Discussionmentioning

confidence: 54%

CTGF Promotes Inflammatory Cell Infiltration of the Renal Interstitium by Activating NF-κB

Sánchez-López¹,

Rayego²,

Rodrigues‐Díez³

et al. 2009

Journal of the American Society of Nephrology

118

100

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Connective tissue growth factor (CTGF) is an important profibrotic factor in kidney diseases. Blockade of endogenous CTGF ameliorates experimental renal damage and inhibits synthesis of extracellular matrix in cultured renal cells. CTGF regulates several cellular responses, including adhesion, migration, proliferation, and synthesis of proinflammatory factors. Here, we investigated whether CTGF participates in the inflammatory process in the kidney by evaluating the nuclear factor-kappa B (NF-B) pathway, a key signaling system that controls inflammation and immune responses. Systemic administration of CTGF to mice for 24 h induced marked infiltration of inflammatory cells in the renal interstitium (T lymphocytes and monocytes/macrophages) and led to elevated renal NF-B activity. Administration of CTGF increased renal expression of chemokines (MCP-1 and RANTES) and cytokines (INF-␥, IL-6, and IL-4) that recruit immune cells and promote inflammation. Treatment with a NF-B inhibitor, parthenolide, inhibited CTGF-induced renal inflammatory responses, including the up-regulation of chemokines and cytokines. In cultured murine tubuloepithelial cells, CTGF rapidly activated the NF-B pathway and the cascade of mitogen-activated protein kinases, demonstrating crosstalk between these signaling pathways. CTGF, via mitogen-activated protein kinase and NF-B activation, increased proinflammatory gene expression. These data show that in addition to its profibrotic properties, CTGF contributes to the recruitment of inflammatory cells in the kidney by activating the NF-B pathway.

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Section: Discussionmentioning

confidence: 54%

CTGF Promotes Inflammatory Cell Infiltration of the Renal Interstitium by Activating NF-κB

Sánchez-López¹,

Rayego²,

Rodrigues‐Díez³

et al. 2009

Journal of the American Society of Nephrology

118

100

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“…JNK is also activated after MI, and inhibition of JNK inhibits IL-6 transcription. 21 Accordingly, we provide evidence that the attenuation of NF-B and JNK activity in IRAK-4 Ϫ/Ϫ mice resulted in decreased inflammation and thus improved host outcome after MI.…”

Section: Irak-4mentioning

confidence: 69%

Survival and Cardiac Remodeling After Myocardial Infarction Are Critically Dependent on the Host Innate Immune Interleukin-1 Receptor-Associated Kinase-4 Signaling

et al. 2009

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Background— The innate immune system greatly contributes to the inflammatory process after myocardial infarction (MI). Interleukin-1 receptor-associated kinase-4 (IRAK-4), downstream of Toll/interleukin-1 receptor signaling, has an essential role in regulating the innate immune response. The present study was designed to determine the mechanism by which IRAK-4 is responsible for the cardiac inflammatory process, which consequently affects left ventricular remodeling after MI. Methods and Results— Experimental MI was created in IRAK-4 −/− and wild-type mice by left coronary ligation. Mice with a targeted deletion of IRAK-4 had an improved survival rate at 4 weeks after MI. IRAK-4 −/− mice also demonstrated attenuated cardiac dilation and decreased inflammation in the infarcted myocardium, which was associated with less proinflammatory and Th1 cytokine expression mediated by suppression of nuclear factor-κB and c-Jun N-terminal kinase activation. IRAK-4 −/− mice had fewer infiltrations of CD45 + leukocytes and CD11c + dendritic cells, inhibition of apoptosis, and reduced fibrosis and nitric oxide production. Cardiac dendritic cells in IRAK-4 −/− mice were relatively immature or functionally naïve after MI in that they demonstrated less cytokine and costimulatory molecule gene expression. Furthermore, IRAK-4 −/− dendritic cells have less mobilization capacity. Transfer of wild type-derived bone marrow dendritic cells into IRAK-4 −/− mice for functional dendritic cell reconstitution negated the survival advantage and reduced the cardiac dilation observed with IRAK-4 −/− mice at 28 days after MI. Conclusions— Deletion of IRAK-4 has favorable effects on survival and left ventricular remodeling after MI through modification of the host inflammatory process by blunting the detrimental bone marrow dendritic cells mobilization after myocardial ischemia.

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“…In contrast, JNK signaling may activate NF-kB, leading to the suppression of apoptosis (Bubici et al, 2004). In addition, TNF-α can promote cell survival, previous studies have shown that IL-6 expression, regulated by JNK, mediates NF-kB-mediated cell survival in renal epithelial cells (de Haij et al, 2005). Our results showed AuNPs inhibited IL-6, stimulated TNF-α, and reduced JNK phosphorylation in U937 cells, while AuNPs did not affect ERK protein (data not shown).…”

Section: Discussionmentioning

confidence: 99%

Effects of silver nanoparticles and gold nanoparticles on IL-2, IL-6, and TNF-α production via MAPK pathway in leukemic cell lines

Parnsamut¹,

Brimson²

2015

Genet. Mol. Res.

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NF-κB Mediated IL-6 Production by Renal Epithelial Cells Is Regulated by C-Jun NH2-Terminal Kinase

Cited by 52 publications

References 46 publications

CTGF Promotes Inflammatory Cell Infiltration of the Renal Interstitium by Activating NF-κB

CTGF Promotes Inflammatory Cell Infiltration of the Renal Interstitium by Activating NF-κB

Survival and Cardiac Remodeling After Myocardial Infarction Are Critically Dependent on the Host Innate Immune Interleukin-1 Receptor-Associated Kinase-4 Signaling

Effects of silver nanoparticles and gold nanoparticles on IL-2, IL-6, and TNF-α production via MAPK pathway in leukemic cell lines

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