PROTEIN KINASE C-Dependent PATHWAY IS CRITICAL FOR THE PRODUCTION OF PRO-INFLAMMATORY CYTOKINES (TNF-α, IL-1β, IL-6)

Kontny, Ewa; Ziolkowska, Maria; Ryzewska, A; Maśliński, Włodzimierz

doi:10.1006/cyto.1998.0496

Cited by 71 publications

(60 citation statements)

References 37 publications

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“…IL-6, however, is not required for the Jurkat cells to produce IL-2 in response to SEE due to the presence of PMA, which is itself a potent accessory signal for T cells (reference 35 and unpublished observation). Rather, these preliminary mechanistic studies suggest that dexamethasone inhibits an as-yet-unknown factor(s) that has corticosteroid response elements (20,25) similar to IL-6. The mechanism for the resistance of the CF B-cell lines to regulation by dexamethasone was not addressed in the present study.…”

Section: Discussionmentioning

confidence: 88%

Superantigens and Cystic Fibrosis: Resistance of Presenting Cells to Dexamethasone

Ben‐Ari

Gozal

Dorio³

et al. 2000

Clin Diagn Lab Immunol

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Section: Discussionmentioning

confidence: 88%

Superantigens and Cystic Fibrosis: Resistance of Presenting Cells to Dexamethasone

Ben‐Ari

Gozal

Dorio³

et al. 2000

Clin Diagn Lab Immunol

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“…Infection of macrophages with M. avium leads to the activation of PKC, and PKC in turn is involved in the activation of many genes, such as TNF-␣, IL-1, and IL-6 (27,28). PKC functions by regulating the activation of transcription factors such as NF-B, c-Fos, and c-Jun (29 -31).…”

Section: Discussionmentioning

confidence: 99%

Regulation of Toll-Like Receptor 2 Expression by Macrophages FollowingMycobacterium aviumInfection

Wang¹,

Lafuse

Zwilling

2000

The Journal of Immunology

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Recent studies have implicated Toll-like receptors (TLR), especially TLR2 and TLR4, as sentinel receptors that signal the interaction of macrophages with bacterial pathogens via a NF-κB-mediated pathway. The regulation of TLR gene expression, however, has not been intensively studied. Here, we report that TLR2 mRNA was induced following infection of murine macrophages with Mycobacterium avium. The changes in TLR2 mRNA correlated with an increase in TLR2 surface expression. Infection with M. avium resulted in a concomitant decrease in TLR4 mRNA. The effect of M. avium infection on TLR2 mRNA appeared to be mediated, in part, by TLR2 because the induction of the mRNA was partially blocked by preincubation of the macrophages with an anti-human TLR2 Ab. In contrast, the effect of LPS stimulation was mediated via TLR4 because infection of macrophages from LPSd mice, which do not express active TLR4, resulted in an increase in TLR2 mRNA, while treatment of macrophages from these mice with LPS failed to induce TLR2 mRNA. Several cytokines, including TNF-α, IL-1α, and GM-CSF, but not IFN-γ, induced TLR2 mRNA. M. avium infection resulted in the induction of TLR2 mRNA by macrophages from both TNFRI knockout and NF-κB p50 knockout mice.

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“…Interestingly, similarly to STAT3, PKC␦ activation in several model systems was shown to mediate signaling by growth factors such as EGF, NGF, PDGF, insulin, TNF␣ and IL-6 (Gliki et al, 2001;Jackson et al, 2001;Jain et al, 1999;Kontny et al, 1999;Novotny-Diermayr et al, 2002;Robin et al, 2004;Shen et al, 2001). However, although STAT3 was shown to be involved in mediating cell growth and oncogenic potential, further studies suggest PKC␦ to be primarily involved in cell differentiation and apoptosis; thus inhibition of PKC␦ activity and loss of PKC␦ during transformation are associated with cell growth and oncogenesis (Fujii et al, 2000;Li et al, 1999;Li et al, 1996b;Lucas and Sanchez-Margalet, 1995).…”

Section: Journal Of Cell Science 119 (3)mentioning

confidence: 99%

The role of protein kinase C δ activation and STAT3 Ser727 phosphorylation in insulin-induced keratinocyte proliferation

Gartsbein

Alt

Hashimoto

et al. 2006

Journal of Cell Science

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Activation of the STAT family of transcription factors is regulated by cytokines and growth factors. STAT tyrosine and serine phosphorylation are linked to the transcriptional activation and function of STAT. We have previously described a unique pathway inducing keratinocyte proliferation, which is mediated by insulin stimulation and depends on protein kinase C δ (PKCδ). In this study, we assessed STAT3 activation downstream of this pathway and characterized the role of PKCδ activation in STAT3 tyrosine and serine phosphorylation and keratinocyte proliferation. Following insulin stimulation, STAT3 interacted with PKCδ but not with any other PKC isoform expressed in skin. Activated forms of PKCδ and STAT3 were essential for insulin-induced PKCδ-STAT3 activation in keratinocyte proliferation. Abrogation of PKCδ activity inhibited insulin-induced STAT3 phosphorylation, PKCδ-STAT3 association and nuclear translocation. In addition, overexpression of STAT3 tyrosine mutant eliminated insulin-induced PKCδ activation and keratinocyte proliferation. Finally, overexpression of a STAT3 serine mutant abrogated insulin-induced STAT3 serine phosphorylation and STAT3-induced keratinocyte proliferation, whereas STAT3 tyrosine phosphorylation was induced and nuclear localization remained intact. This study indicates that PKCδ activation is a primary regulator of STAT3 serine phosphorylation and that PKCδ is essential in directing insulin-induced signaling in keratinocyte proliferation.

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PROTEIN KINASE C-Dependent PATHWAY IS CRITICAL FOR THE PRODUCTION OF PRO-INFLAMMATORY CYTOKINES (TNF-α, IL-1β, IL-6)

Cited by 71 publications

References 37 publications

Superantigens and Cystic Fibrosis: Resistance of Presenting Cells to Dexamethasone

Superantigens and Cystic Fibrosis: Resistance of Presenting Cells to Dexamethasone

Regulation of Toll-Like Receptor 2 Expression by Macrophages FollowingMycobacterium aviumInfection

The role of protein kinase C δ activation and STAT3 Ser727 phosphorylation in insulin-induced keratinocyte proliferation

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