Activation of NF-κB in Normal Rat Kidney Epithelial (NRK52E) Cells Is Mediated via a Redox-Insensitive, Calcium-Dependent Pathway

Woods, James S.; Ellis, Maureen E.; Dieguez-Acuña, Francisco J.; Corral, J.

doi:10.1006/taap.1998.8583

Cited by 41 publications

(25 citation statements)

References 48 publications

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“…This may imply that defective LPS signaling may play a role in the observed inability of PhoP c to elicit calcium mobilization and subsequent events. Recent reports have demonstrated Ca 2+ -dependent signaling elicited by LPS in several host cell types (50,51). We also note that IκB-α degradation or activation of IκB kinase in response to LPS has been reported to occur in monocytic cells (52,53) with kinetics similar to the Salmonella-(and carbachol-) mediated responses reported herein (in epithelial cells).…”

Section: Discussionsupporting

confidence: 83%

Salmonella typhimurium induces epithelial IL-8 expression via Ca2+-mediated activation of the NF-κB pathway

Gewirtz¹,

Rao²,

Simon³

et al. 2000

J. Clin. Invest.

200

170

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Section: Discussionsupporting

confidence: 83%

Salmonella typhimurium induces epithelial IL-8 expression via Ca2+-mediated activation of the NF-κB pathway

Gewirtz¹,

Rao²,

Simon³

et al. 2000

J. Clin. Invest.

200

170

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“…Furthermore, pretreatment with intracellular calcium chelator BAPTA-AM attenuated the TNF-α- or IL-1β-induced NF-ĸB activation, suggesting that TNF-α- or IL-1β-induced NF-ĸB activation in human mesangial cells was mediated, at least in part, through intracellular calcium. In line with our results, Wood et al [17] reported that lipopolysaccharide-induced NF-ĸB activation in normal rat kidney epithelial cells was mediated via a redox-insensitive, calcium-dependent pathway. …”

Section: Discussionsupporting

confidence: 82%

Proinflammatory Cytokine-Induced NF-κB Activation in Human Mesangial Cells Is Mediated through Intracellular Calcium but Not ROS: Effects of Silymarin

Chang

Kim

et al. 2006

Nephron Exp Nephrol

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Background: It is not fully understood whether intracellular calcium and/or reactive oxygen species (ROS) are involved in nuclear factor-ĸB (NF-ĸB) activation by proinflammatory cytokines. Silymarin exhibits anti-inflammatory and antioxidant effects but the effect of silymarin in human mesangial cells is largely unknown. Method: NF-ĸB binding activity was measured by electrophoretic mobility shift assay. Intracellular calcium was monitored by confocal microscopy using Fluo-3 and intracellular ROS production was determined by flow cytometry. Monocyte chemoattractant protein-1 (MCP-1) expression was measured by Northern blot analysis and ELISA. Results: NF-ĸB was activated within 30 min by tumor necrosis factor-α (TNF-α) or interleukin-1β (IL-1β). Intracellular ROS was not produced until 30 min and also antioxidants such as N-acetylcysteine and tiron had no effect on the TNF-α- or IL-1β-induced NF-ĸB activation. Intracellular calcium was increased by TNF-α and IL-1β. Furthermore, a calcium chelator, BAPTA-AM, attenuated the NF-ĸB activation. Silymarin dose-dependently inhibited the TNF-α- or IL-1β-induced NF-ĸB activation and MCP-1 expression. Silymarin also inhibited TNF-α-induced intracellular calcium. Conclusions: Induction of NF-ĸB within 30 min by TNF-α- and IL-1β was mediated through intracellular calcium but not ROS. Silymarin inhibited TNF-α-induced calcium-dependent NF-ĸB activation irrespective of its antioxidant effect.

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“…It also remains a possibility that CI acts indirectly, through the induced secretion of biological agents that, in turn, act in an autocrine fashion to promote differentiation. However, thapsigargin, a compound that causes a rapid efflux of Ca 2ϩ from the endoplasmic reticulum, has been shown, as a single agent, to activate NF-B in HeLa cells (35), normal renal tubular epithelial cells (36), and pancreatic lobules (37). This activation is inhibited by pyrrolidine dithiocarbamate and therefore requires the presence of reactive oxygen intermediates.…”

Section: Discussionmentioning

confidence: 99%

Bacterial Lipopolysaccharide, TNF-α, and Calcium Ionophore Under Serum-Free Conditions Promote Rapid Dendritic Cell-Like Differentiation in CD14+ Monocytes Through Distinct Pathways That Activate NF-κB

Lyakh

Koski

Telford

et al. 2000

The Journal of Immunology

105

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To facilitate the study of signaling pathways involved in myeloid dendritic cell (DC) differentiation, we have developed a serum-free culture system in which human CD14+ peripheral blood monocytes differentiate rapidly in response to bacterial LPS, TNF-α, or calcium ionophore (CI). Within 48–96 h, depending on the inducing agent, the cells acquire many immunophenotypical, morphological, functional, and molecular properties of DC. However, there are significant differences in the signaling pathways used by these agents, because 1) LPS-induced, but not CI-induced, DC differentiation required TNF-α production; and 2) cyclosporin A inhibited differentiation induced by CI, but not that induced by LPS. Nevertheless, all three inducing agents activated members of the NF-κB family of transcription factors, including RelB, suggesting that despite differences in upstream elements, the signaling pathways all involve NF-κB. In this report we also demonstrate and offer an explanation for two observed forms of the RelB protein and show that RelB can be induced in myeloid cells, either directly or indirectly, through a calcium-dependent and cyclosporin A-sensitive pathway.

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Activation of NF-κB in Normal Rat Kidney Epithelial (NRK52E) Cells Is Mediated via a Redox-Insensitive, Calcium-Dependent Pathway

Cited by 41 publications

References 48 publications

Salmonella typhimurium induces epithelial IL-8 expression via Ca2+-mediated activation of the NF-κB pathway

Salmonella typhimurium induces epithelial IL-8 expression via Ca2+-mediated activation of the NF-κB pathway

Proinflammatory Cytokine-Induced NF-κB Activation in Human Mesangial Cells Is Mediated through Intracellular Calcium but Not ROS: Effects of Silymarin

Bacterial Lipopolysaccharide, TNF-α, and Calcium Ionophore Under Serum-Free Conditions Promote Rapid Dendritic Cell-Like Differentiation in CD14+ Monocytes Through Distinct Pathways That Activate NF-κB

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