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• W2147645315 endingPage "33" @default.
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• W2147645315 abstract "Inflammatory mediators, including cytokines, contribute to neuronal and axonal dysfunction and cell death. To examine the roles of cytokines in pathogenesis and regeneration in the central nervous system (CNS), we analyzed effects of cytokines on early gene regulation (6 h) in neuronal cultures, employing gene arrays. Our hypothesis is that neuronal gene expression is differentially regulated in vitro by cytokine mixtures typical of Th1 and Th2 T cells and monocytes/macrophages (M/M). Th1 and M/M cytokines showed similar patterns for regulation of numerous pathways including cytokine-receptor interactions, MAP kinase, toll like receptors, apoptosis, PPAR signaling, cell adhesion molecules (CAMS), antigen processing, adipocytokine, and JAK-STAT signaling. M/M cytokines uniquely regulated genes in T cell, B cell and ECM receptor signaling pathways. Th2 cytokines had few effects on pathways regulated by Th1 and MM cytokines, but uniquely regulated genes related to neuroactive ligand-receptors and calcium. Th1 and MM cytokines markedly upregulated a wide array of cytokine-related genes. Notably, M/M cytokines uniquely upregulated G-CSF, GM-CSF, CXCL5 and lymphotactin (Xcl1). Th2 cytokines did not upregulate cytokine-related genes, with the exception of CCL11 and FMS-like tyrosine kinase 1, a VEGF receptor. In neuroactive ligand-receptor pathways, Th1 and M/M cytokines upregulated gene expression for tryptophan hydroxylase. Th1 cytokines upregulated gene expression for GABA A receptor, delta, while Th2 cytokines downregulated GABA A receptor, gamma 3. Significant changes occurred in several genes in the wnt and Notch signaling pathways, which are highly conserved and play critical roles in neuronal and glial differentiation. In the ubiquitin–proteasome pathway, proinflammatory cytokine mixtures induced upregulation of several genes, notably ubiquitin D (Ubd/FAT10), ubiquitin ligase and several proteasomal proteins. In agreement with microarray results, QRT-PCR showed marked upregulation of gene expression for Ubd with Th1 and M/M, for transglutaminase 2 with M/M, and for arginase 1 with Th2 cytokines. Expression of Ubd in the nervous system has not been previously reported. Both message and protein for Ubd are expressed in neurons, and upregulated by pro-inflammatory cytokines. Transglutaminase 2 has been implicated in neurodegenerative diseases, and proposed as a therapeutic target. Upregulation of arginase by Th2 cytokines could be potentially neuroprotective by decreasing NO generation and enhancing neurite outgrowth. Our analysis of changes in neuronal gene expression at the time of initial exposure to an abnormal cytokine milieu provides the opportunity to identify early changes that could be reversed to prevent later irreversible neuronal damage and death in multiple sclerosis and other CNS diseases." @default.
• W2147645315 created "2016-06-24" @default.
• W2147645315 creator A5009994219 @default.
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• W2147645315 creator A5066697011 @default.
• W2147645315 creator A5068084952 @default.
• W2147645315 creator A5083845228 @default.
• W2147645315 date "2011-09-01" @default.
• W2147645315 modified "2023-10-15" @default.
• W2147645315 title "Cytokines regulate neuronal gene expression: Differential effects of Th1, Th2 and monocyte/macrophage cytokines" @default.
• W2147645315 cites W1270085290 @default.
• W2147645315 cites W1500225421 @default.
• W2147645315 cites W1525813631 @default.
• W2147645315 cites W1595078459 @default.
• W2147645315 cites W1862266358 @default.
• W2147645315 cites W1878384586 @default.
• W2147645315 cites W1958592565 @default.
• W2147645315 cites W1964163541 @default.
• W2147645315 cites W1967803088 @default.
• W2147645315 cites W197245174 @default.
• W2147645315 cites W1972559333 @default.
• W2147645315 cites W1974366107 @default.
• W2147645315 cites W1976025359 @default.
• W2147645315 cites W1978483334 @default.
• W2147645315 cites W1980008834 @default.
• W2147645315 cites W1981642191 @default.
• W2147645315 cites W1984188855 @default.
• W2147645315 cites W1988771698 @default.
• W2147645315 cites W1991634033 @default.
• W2147645315 cites W1995796870 @default.
• W2147645315 cites W1998299241 @default.
• W2147645315 cites W1999110803 @default.
• W2147645315 cites W2001062595 @default.
• W2147645315 cites W2003674452 @default.
• W2147645315 cites W2004508412 @default.
• W2147645315 cites W2005353940 @default.
• W2147645315 cites W2005789443 @default.
• W2147645315 cites W2006178657 @default.
• W2147645315 cites W2009885803 @default.
• W2147645315 cites W2011813413 @default.
• W2147645315 cites W2015190612 @default.
• W2147645315 cites W2016111184 @default.
• W2147645315 cites W2017574176 @default.
• W2147645315 cites W2018226150 @default.
• W2147645315 cites W2019926860 @default.
• W2147645315 cites W2021626693 @default.
• W2147645315 cites W2021898378 @default.
• W2147645315 cites W2025732446 @default.
• W2147645315 cites W2026287451 @default.
• W2147645315 cites W2028862619 @default.
• W2147645315 cites W2029327879 @default.
• W2147645315 cites W2030908648 @default.
• W2147645315 cites W2031611126 @default.
• W2147645315 cites W2031809301 @default.
• W2147645315 cites W2032989272 @default.
• W2147645315 cites W2034415508 @default.
• W2147645315 cites W2034417232 @default.
• W2147645315 cites W2034947823 @default.
• W2147645315 cites W2035098555 @default.
• W2147645315 cites W2037965052 @default.
• W2147645315 cites W2041104342 @default.
• W2147645315 cites W2045901798 @default.
• W2147645315 cites W2047062145 @default.
• W2147645315 cites W2049105252 @default.
• W2147645315 cites W2049187627 @default.
• W2147645315 cites W2049191190 @default.
• W2147645315 cites W2052644415 @default.
• W2147645315 cites W2053189124 @default.
• W2147645315 cites W2056019648 @default.
• W2147645315 cites W2060493925 @default.
• W2147645315 cites W2061891340 @default.
• W2147645315 cites W2062942165 @default.
• W2147645315 cites W2063909802 @default.
• W2147645315 cites W2065200510 @default.
• W2147645315 cites W2066878270 @default.
• W2147645315 cites W2070222386 @default.
• W2147645315 cites W2071151220 @default.
• W2147645315 cites W2072870301 @default.
• W2147645315 cites W2072959439 @default.
• W2147645315 cites W2074558188 @default.
• W2147645315 cites W2074795981 @default.
• W2147645315 cites W2075126054 @default.
• W2147645315 cites W2075742252 @default.
• W2147645315 cites W2078945968 @default.
• W2147645315 cites W2079276179 @default.
• W2147645315 cites W2083393999 @default.
• W2147645315 cites W2084210959 @default.
• W2147645315 cites W2088559288 @default.
• W2147645315 cites W2089204174 @default.
• W2147645315 cites W2089819518 @default.
• W2147645315 cites W2092902275 @default.
• W2147645315 cites W2093803567 @default.
• W2147645315 cites W2096277075 @default.
• W2147645315 cites W2097631517 @default.
• W2147645315 cites W2097632269 @default.
• W2147645315 cites W2100602740 @default.
• W2147645315 cites W2106502610 @default.

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