Differential Regulation of Interleukin-8 and Intercellular Adhesion Molecule-1 by H2O2 and Tumor Necrosis Factor-α in Endothelial and Epithelial Cells

Lakshminarayanan, Venkatesh; Beno, David W. A.; Costa, Robert H.; Roebuck, Kenneth A.

doi:10.1074/jbc.272.52.32910

Cited by 152 publications

(125 citation statements)

References 76 publications

Supporting

Mentioning

112

Contrasting

Unclassified

Order By: Relevance

“…Enhanced MCP-1 and MIP-2 expression in Lm-infected mice treated with the PTP inhibitor bpV(phen) has been reported previously [11]. Additionally, TNF-a, IL-1b and IL-6 have been recognized as inducers of IL-8, MCP-1 and MIP-2 expression [38][39][40]. Therefore, the elevated generation of these pro-inflammatory cytokines paralleled by increased chemokine expression during Lm infection in the absence of SHP-1 could explain in part the tremendous cellular recruitment of both monocytes/MU and neutrophils observed in SHP-1-deficient mice.…”

Section: Discussionmentioning

confidence: 60%

Regulation of theLeishmania-induced innate inflammatory response by the protein tyrosine phosphatase SHP-1

et al. 2005

View full text Add to dashboard Cite

Modulation of the phagocyte protein tyrosine phosphatase (PTP) SHP-1 by the parasite Leishmania favors its survival and propagation within its mammalian host. In vivo, the absence of SHP-1 leads to virtually absent footpad swelling, accompanied by enhanced inducible nitric oxide synthase expression. In this study, using an air pouch model, we show that viable motheaten SHP-1-deficient mice harbored a stronger inflammatory response against Leishmania infection than wild-type mice. This response was portrayed by higher pro-inflammatory cytokine (TNF-a, IL-1b and IL-6) expression and secretion and by greater chemokine and chemokine receptor expression. These inflammatory molecules were probably responsible for the stronger cellular recruitment, mainly of neutrophils, seen at the site of infection in viable motheaten mice within 6 h post inoculation. We also provide strong evidence that protein tyrosine phosphatases in general, and SHP-1 in particular, are important regulators of chemokine gene expression. Overall, this study suggests that the ability of Leishmania to induce SHP-1 activity in its host allows the taming of an otherwise strong innate inflammatory response that would be detrimental for its survival and progression.

show abstract

Section: Discussionmentioning

confidence: 60%

Regulation of theLeishmania-induced innate inflammatory response by the protein tyrosine phosphatase SHP-1

et al. 2005

View full text Add to dashboard Cite

show abstract

“…Though it is commonly reported that 1-2% of electron flow on the ETC leads to ROS production, more recent reports show this value to be as low as 0.15%, depending on the carbon source being oxidized [36,37]. A high concentration of mitochondrial SOD ensures no significant O 2 .− accumulation beyond its initial site of production and allows for the generation of H 2 O 2 which has second messenger effects in the cytosol [31,[38][39][40]. The endoplasmic reticulum (ER) is another cellular source of ROS where resident cytochrome P-450 and b 5 family members oxidize unsaturated fatty acids and xenobiotics to generate O 2 .− and H 2 O 2 [41][42][43].…”

Section: Types and Sources Of Cellular Rosmentioning

confidence: 99%

Reactive oxygen species and cellular oxygen sensing

Cash

Pan

Simon

2007

Free Radical Biology and Medicine

164

100

View full text Add to dashboard Cite

Many organisms activate adaptive transcriptional programs to help them cope with decreased oxygen levels, or hypoxia, in their environment. These responses are triggered by various oxygen sensing systems in bacteria, yeast and metazoans. In metazoans, the hypoxia inducible factors (HIFs) mediate the adaptive transcriptional response to hypoxia by upregulating genes involved in maintaining bioenergetic homeostasis. The HIFs in turn are regulated by HIF-specific prolyl hydroxlase activity, which is sensitive to cellular oxygen levels and other factors such as tricarboxylic acid cycle metabolites and reactive oxygen species (ROS). Establishing a role for ROS in cellular oxygen sensing has been challenging since ROS are intrinsically unstable and difficult to measure. However, recent advances in fluorescence energy transfer resonance (FRET)-based methods for measuring ROS are alleviating some of the previous difficulties associated with dyes and luminescent chemicals. In addition, new genetic models have demonstrated that functional mitochondrial electron transport and associated ROS production during hypoxia are required for HIF stabilization in mammalian cells. Current efforts are directed at how ROS mediate prolyl hydroxylase activity and hypoxic HIF stabilization. Progress in understanding this process has been enhanced by the development of the FRET-based ROS probe, an vivo prolyl hydroxylase reporter and various genetic models harboring mutations in components of the mitochondrial electron transport chain.

show abstract

“…Angiotensin II can also stimulate NF-kB translocation to the nucleus resulting in VCAM-1 expression (Pueyo et al 2000) and inflammation. In a complimentary pathway, TNF-A and PKC also contribute to the formation of ROS, again resulting in NF-kB activation as well as ICAM-1 expression (Lakshminarayanan et al 1997;True et al 2000;Ahmad et al 2002). In a review by…”

Section: Inflammationmentioning

confidence: 99%

“…Additional implicated factors include Fe 2+ (Chen et al 2004), MCP-1 gene expression (Chen et al 2004), and RAC-1 (Lakshminarayanan et al 1997;Ahmad et al 2002;Chen et al 2004) …”

Section: Inflammationmentioning

confidence: 99%