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Suppressor of cytokine signaling and accelerated atherosclerosis in kidney disease

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Wesoly J., Sikorski K., Lee C.-K., Bluyssen H. A. R.
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2010
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vol. 57
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issue 3
251-260
EN
The prevalence of cardiovascular disease in patients with renal failure is extremely high and accounts for a large part of the morbidity and mortality. Inflammation participates importantly in host defense against infectious agents and injury, but also contributes to the pathophysiology of many diseases, including cardiovascular atherosclerosis, which is a main problem in patients with renal failure. Recruitment of blood leukocytes to the injured vascular endothelium characterizes the initiation and progression of atherosclerosis and involves many inflammatory mediators, modulated by cells of both innate and adaptive immunity. Excessive inflammatory and immune responses, communicated by these different cell types, are driven by inflammatory cytokines that promote associated tissue damage if cytokine signaling pathways remain unregulated. Thus, pathways capable of suppressing proinflammatory cytokine signaling hold the potential to limit life-threatening cardiovascular events caused by atherogenesis. Suppressor of cytokine signaling (SOCS) are a family of intracellular proteins, several of which have emerged as key physiological regulators of cytokine-mediated homeostasis, including innate and adaptive immunity. Accumulating evidence supports the idea that dysregulation of cytokine signaling by differential SOCS expression is involved in the pathogenesis of various inflammatory, and immunological diseases, including atherosclerosis. Based on recent observations, in which SOCS expression levels are profoundly altered in kidney disease, we discuss the possibilities of SOCS as new intracellular markers of inflammation as well as their potential atherogenic properties in renal failure related cardiovascular disease.
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STAT activation and differential complex formation dictate selectivity of interferon responses

100%
Wesoly J., Szweykowska-Kulinska Z., Bluyssen H. A. R.
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2007
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vol. 54
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issue 1
27-38
EN
Interferons (IFNs) induce gene expression by phosphorylating latent transcription factors belonging to the signal transducer and activator of transcription (STAT) family, mediated by janus kinases (Jaks). STAT dimers directly activate genes containing the IFNγ activation site (GAS) DNA element, with different STAT proteins displaying slightly different intrinsic DNA binding specificities. The combinatorial association of STATs with the additional DNA binding adaptor protein interferon regulatory factor (IRF)9 expands the range of enhancer elements that can be targeted by the JAK-STAT pathway to interferon-stimulated response element (ISRE) and IRF response element (IRE). Based on the amino-acid sequence similarity within the IRF family and functional overlap with the STAT family, in this paper we hypothesize that other IRF members could serve as adapter proteins for the STATs during IFN responses to redirect them to subsets of ISRE, GAS and/or IRE-containing IFN-stimulated genes (ISGs). In addition, the fact that STAT2 homodimers are not capable of binding consensus GAS sites leaves the possibility for a novel type of DNA-binding site bound by STAT2 homodimers and potentially other STAT complexes.
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