ERK 1/2- and JNKs-dependent Synthesis of Interleukins 6 and 8 by Fibroblast-like Synoviocytes Stimulated with Protein I/II, a Modulin from Oral Streptococci, Requires Focal Adhesion Kinase

Neff, L.; Zeisel, Mirjam B.; Druet, Vanessa A.; Takeda, Ken; Klein, Jean‐Paul; Sibilia, Jean; Wachsmann, Dominique

doi:10.1074/jbc.m212065200

Cited by 41 publications

(41 citation statements)

References 48 publications

(43 reference statements)

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“…FAK ϩ/ϩ cells were transfected with FRNK-YCam (a generous gift from K. Takeda) by the calcium phosphate method as previously described (6). Following transfection, cells were rinsed and then cultured in complete DMEM medium containing geneticin (1.5 mg/ml) for 2 wk.…”

Section: Transfectionsmentioning

confidence: 99%

“…FLSs (5 ϫ 10 3 cells per well) were grown to confluence in 96-well plates and serum-starved for 24 h before activation experiments. FAK ϩ/ϩ and FAK Ϫ/Ϫ primary mouse embryo fibroblasts (American Type Culture Collection; CRL-2644 and -2645) were cultured as previously described (6). Cells were plated in 96-well plates (5 ϫ 10 4 cells per well) and serum-starved 24 h before activation experiments.…”

Section: Cell Culturesmentioning

confidence: 99%

“…GFP was used to determine the transfection efficiency. Transient transfection of FLSs was performed using the Nucleofector kit as previously described (6). Cells were then plated in 96-well plates (5 ϫ 10 4 cells per well) before activation experiments.…”

Section: Transfectionsmentioning

confidence: 99%

“…Proteins from cell lysates were subjected to SDS-PAGE and transferred electrophoretically to nitrocellulose membranes. FAK was detected using anti-FAK (pY397; BioSource; Cliniscience) and anti-FAK polyclonal Abs (BD Pharmingen; Cliniscience) as previously described (6).…”

Section: Western Blotmentioning

confidence: 99%

“…Protein I/II, a cell wall component from oral streptococci, binding to integrin ␣ 5 ␤ 1 induces the production of inflammatory mediators such as IL-6 and IL-8 by human monocytes, epithelial cells, endothelial cells, and fibroblasts (5,6). The signaling events leading to this cytokine release involve FAK, ERK1/2, and JNKs as well as AP-1-binding activity and nuclear translocation of NF-B (6,7). FAK is an interesting candidate to link bacterial detection, initiation of proinflammatory responses, and cell entry, because FAK is involved in invasin-mediated bacterial uptake (8).…”

mentioning

confidence: 99%

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Cross Talk between MyD88 and Focal Adhesion Kinase Pathways

Zeisel

Druet

Sibilia

et al. 2005

The Journal of Immunology

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Focal adhesion kinase (FAK) is a nonreceptor protein tyrosine kinase involved in signaling downstream of integrins, linking bacterial detection, cell entry, and initiation of proinflammatory response through MAPKs and NF-κB activation. In this study, using protein I/II from Streptococcus mutans as a model activator of FAK, we investigated the potential link between FAK and TLR pathways. Using macrophages from TLR- or MyD88-deficient mice, we report that MyD88 plays a major role in FAK-dependent protein I/II-induced cytokine release. However, response to protein I/II stimulation was independent of TLR4, TLR2, and TLR6. The data suggest that there is a cross talk between FAK and MyD88 signaling pathways. Moreover, MyD88-dependent, LPS-induced IL-6 secretion by human and murine fibroblasts required the presence of FAK, confirming that MyD88 and FAK pathways are interlinked.

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Section: Transfectionsmentioning

confidence: 99%

Section: Cell Culturesmentioning

confidence: 99%

Section: Transfectionsmentioning

confidence: 99%

Section: Western Blotmentioning

confidence: 99%

mentioning

confidence: 99%

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Cross Talk between MyD88 and Focal Adhesion Kinase Pathways

Zeisel

Druet

Sibilia

et al. 2005

The Journal of Immunology

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Emerging issues in smoking among adolescent and adult cancer survivors

Klosky

Tyc

Garces-Webb

et al. 2007

Cancer

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The number of cancer survivors is significantly increasing, thereby prioritizing the importance of identifying and preventing adverse health outcomes within this high-risk population. Cigarette smoking is of particular salience as it places both adolescents and adults with a cancer history at risk for various health problems, including second malignancies. The purpose of this article is to provide a comprehensive review of the smoking literature as it relates to adolescents and adults on-treatment and surviving cancer. In particular, the article reviews the prevalence, risk factors, and health outcomes associated with smoking, in addition to the prevention and smoking cessation interventions available to adolescent and adult oncology patients. Furthermore, efficacious cessation strategies have recently emerged from the smoking literature in healthy populations, and their application to oncology populations is discussed.

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FAK activation is required for TNF‐α‐induced IL‐6 production in myoblasts

Tseng

Tang

2010

Journal Cellular Physiology

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Tumor necrosis factor-alpha (TNF-alpha) is a pleiotropic cytokine produced by activated macrophages. IL-6 is a multifunctional cytokine that plays a central role in both innate and acquired immune responses. We investigated the signaling pathway involved in IL-6 production stimulated by TNF-alpha in cultured myoblasts. TNF-alpha caused concentration-dependent increases in IL-6 production. TNF-alpha-mediated IL-6 production was attenuated by focal adhesion kinase (FAK) mutant and siRNA. Pretreatment with phosphatidylinositol 3-kinase inhibitor (PI3K; Ly294002 and wortmannin), Akt inhibitor, NF-kappaB inhibitor (pyrrolidine dithiocarbamate, PDTC), and IkappaB protease inhibitor (L-1-tosylamido-2-phenyl phenylethyl chloromethyl ketone, TPCK) also inhibited the potentiating action of TNF-alpha. TNF-alpha increased the FAK, PI3K, and Akt phosphorylation. Stimulation of myoblasts with TNF-alpha activated IkappaB kinase alpha/beta (IKKalpha/beta), IkappaBalpha phosphorylation, p65 phosphorylation, and kappaB-luciferase activity. TNF-alpha mediated an increase of kappaB-luciferase activity which was inhibited by Ly294002, wortmannin, Akt inhibitor, PDTC and TPCK or FAK, PI3K, and Akt mutant. Our results suggest that TNF-alpha increased IL-6 production in myoblasts via the FAK/PI3K/Akt and NF-kappaB signaling pathway.

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ERK 1/2- and JNKs-dependent Synthesis of Interleukins 6 and 8 by Fibroblast-like Synoviocytes Stimulated with Protein I/II, a Modulin from Oral Streptococci, Requires Focal Adhesion Kinase

Cited by 41 publications

References 48 publications

Cross Talk between MyD88 and Focal Adhesion Kinase Pathways

Cross Talk between MyD88 and Focal Adhesion Kinase Pathways

Emerging issues in smoking among adolescent and adult cancer survivors

FAK activation is required for TNF‐α‐induced IL‐6 production in myoblasts

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