Transcriptional regulation of human CC chemokine CCL15 gene by NF-κB and AP-1 elements in PMA-stimulated U937 monocytoid cells

Shin, Yong‐Hyun; Son, Kyung-No; Lee, Guy Wilhem; Kwon, Byoung S.; Kim, Jiyoung

doi:10.1016/j.bbaexp.2005.11.001

Cited by 9 publications

(8 citation statements)

References 25 publications

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“…4C). To confirm the difference in AP-1 activation between gingival fibroblasts and U937 cells, cells were treated with phorbol-12-myristate-13-acetate (PMA), a compound known to activate AP-1 activity in U937 cells previously [16]. Results confirmed that PMA stimulated AP-1 activity in U937 cells as reported, but it did not stimulate AP-1 activity in gingival fibroblasts (Fig.…”

Section: Resultssupporting

confidence: 78%

Different signaling mechanisms regulating IL-6 expression by LPS between gingival fibroblasts and mononuclear cells: seeking the common target

Jin

Sundararaj

Samuvel

et al. 2012

Clinical Immunology

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To reduce connective tissue IL-6 level stimulated by LPS, it is essential to control IL-6 expression in both mononuclear cells and fibroblasts. However, it is unclear whether the regulatory mechanisms for both cells are similar or not. In this study, we found that signaling pathways mediating LPS-stimulated IL-6 in mononuclear U937 cells and fibroblasts were different. Furthermore, our studies showed that while LPS activated AP-1 and NFκB in U937 cells, it only activated NFκB in fibroblasts. Analysis of nuclear AP-1 subunits showed that LPS stimulated c-Fos, Fra-1 and Jun D activities in U937 cells, but not fibroblasts. The lack of ERK involvement in LPS-stimulated IL-6 in fibroblasts was further supported by the observations that simvastatin, which is known to target ERK-AP-1, failed to inhibit LPS-stimulated IL-6 by fibroblasts. Finally, we showed that targeting NFκB pathway was highly effective in inhibition of LPS-stimulated IL-6 in coculture of U937 cells and fibroblasts.

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Section: Resultssupporting

confidence: 78%

Different signaling mechanisms regulating IL-6 expression by LPS between gingival fibroblasts and mononuclear cells: seeking the common target

Jin

Sundararaj

Samuvel

et al. 2012

Clinical Immunology

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“…Moreover, NF-B can regulate the Lkn-1-induced protein expression of the human leucine zipper protein [15], which binds CCR1 and induces the migration of THP-1 cells upon Lkn-1 stimulation without affecting the chemotactic activities of other CCR1 agonists [16]. Expressions of Lkn-1, MIP-1␣/CCL3 (a CCR1 agonist), RANTES/ CCL5 (another CCR1 agonist), MCP-1, GRO-␣, and IL-8/ CXCL8 (a CXCR1 and CXCR2 agonist) are regulated in part by the activation of NF-B [8,[17][18][19][20], which can also mediate the chemotaxis of breast cancer cells by up-regulating the expression of CXCR4 directly [21]. Although che-mokine receptors are typically characterized as G i -coupled receptors, there is substantial evidence to suggest that chemokines can mediate NF-B activation through PTX-insensitive G proteins.…”

Section: Introductionmentioning

confidence: 99%

CCR1-mediated activation of nuclear factor-κB in THP-1 monocytic cells involves pertussis toxin-insensitive Gα14 and Gα16 signaling cascades

Lee

Wong

2009

Journal of Leukocyte Biology

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Agonists of CC chemokine receptor CCR1 contribute to the pathogenesis of autoimmune and other inflammatory diseases, possibly via the regulation of the transcription factor NF-kappaB. CCR1 and CCR2b have been demonstrated to use PTX-insensitive Galpha(14) and Galpha(16) to stimulate PLCbeta in cotransfected cells, and Galpha(14) and Galpha(16) are capable of activating NF-kappaB. The coexpression of Galpha(14), Galpha(16), and CCR1 in human monocytic THP-1 cells suggests that CCR1 may use Galpha(14) or Galpha(16) to induce NF-kappaB activation. Here, we demonstrated that a CCR1 agonist, Lkn-1, stimulated NF-kappaB phosphorylation via PTX-insensitive G proteins in THP-1 cells. Lkn-1 also mediated IKK/NF-kappaB phosphorylations in HEK293 cells overexpressing CCR1 and Galpha(14/16). Using various kinase inhibitors, Raf-1, MEK1/2, PLCbeta, PKC, CaM, CaMKII, and c-Src were found to participate in Lkn-1-stimulated IKK/NF-kappaB phosphorylations in THP-1 and transfected HEK293 cells. Although c-Jun N-terminal kinase and p38 MAPK were activated by Lkn-1, they were not required in Lkn-1-induced IKK phosphorylation. The ability of CCR1 to signal through Galpha(14/16) thus provides a linkage for chemokines to regulate NF-kappaB-dependent responses.

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“…Nuclear extracts from mouse macrophage RAW264.7 cells were prepared as previously described (8). EMSA was performed as described previously.…”

Section: Electrophoretic Mobility Shift Assay (Emsa)mentioning

confidence: 99%

“…Total RNA (2 μg) was reverse transcribed using M-MuLV reverse transciptase (Fermentas Life Sciecne) and PCR was performed as previously described using specific primers (8). Real time PCRs were performed by a fluorescence detection method using the LightCycler System with a First-Start DNA Master SYBR Green I kit (Roche Diagnostics) as described previously (29).…”

Section: Reverse Transcriptase-pcr Analysis and Real-time Pcrmentioning

confidence: 99%

“…The inflammatory response is accompanied by an upregulation of cytokines, growth factors, inducible NO synthase (iNOS) and many other enzymes and factors (4)(5)(6) that may contribute to the initiation and promotion of tumor formation. Pro-inflammatory genes, such as TNF-α and iNOS are induced by a wide range of signals, including lipopolysaccharides (LPS), phorbol esters and growth factors, through the activation of AP-1 and NF-κB (7,8).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Suppressive effects of Lithospermum erythrorhizon extracts on lipopolysaccharide-induced activation of AP-1 and NF-κB via mitogen-activated protein kinase pathways in mouse macrophage cells

Han¹,

Kwon²,

Lee³

et al. 2008

BMB Reports

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Transcriptional regulation of human CC chemokine CCL15 gene by NF-κB and AP-1 elements in PMA-stimulated U937 monocytoid cells

Cited by 9 publications

References 25 publications

Different signaling mechanisms regulating IL-6 expression by LPS between gingival fibroblasts and mononuclear cells: seeking the common target

Different signaling mechanisms regulating IL-6 expression by LPS between gingival fibroblasts and mononuclear cells: seeking the common target

CCR1-mediated activation of nuclear factor-κB in THP-1 monocytic cells involves pertussis toxin-insensitive Gα14 and Gα16 signaling cascades

Suppressive effects of Lithospermum erythrorhizon extracts on lipopolysaccharide-induced activation of AP-1 and NF-κB via mitogen-activated protein kinase pathways in mouse macrophage cells

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