Comparison of Gene Expression Patterns Induced by Treatment of Human Umbilical Vein Endothelial Cells with IFN-α2b vs. IFN-β1a: Understanding the Functional Relationship Between Distinct Type I Interferons That Act Through a Common Receptor

At the replication fork, nucleosomes, transcription factors and RNA polymerases are stripped off the DNA, the DNA double strands are unzipped and DNA methylation marks may be erased. Therefore DNA replication is both a ‘curse’ and ‘bliss’ for the epigenome, as it disrupts its stability by causing chromatin perturbations, yet it offers an opportunity to initiate changes in chromatin architecture and gene expression patterns, especially during development. Thus the DNA replication site is a critical point for regulation. It has become apparent that there is a close functional relationship between those factors that regulate transcriptional competence and the DNA replication programme. In this review we discuss novel insights into how chromatin-remodelling factors at replication sites are involved in both the maintenance and regulation of transcriptional states.

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Differential MicroRNA Profiling in a Cellular Hypoxia Reoxygenation Model upon Posthypoxic Propofol Treatment Reveals Alterations in Autophagy Signaling Network

Oxidative Medicine and Cellular Longevity ◽

10.1155/2013/378484 ◽

2013 ◽

Vol 2013 ◽

pp. 1-11 ◽

Cited By ~ 20

Author(s):

Zhuo Chen ◽

Zhe Hu ◽

Zhiqi Lu ◽

Shuyun Cai ◽

Xiaoxia Gu ◽

...

Keyword(s):

Gene Expression ◽

Mirna Expression ◽

Umbilical Vein ◽

Expression Patterns ◽

Global Perspective ◽

Genome Wide ◽

Cellular Hypoxia ◽

Umbilical Vein Endothelial Cells ◽

Microrna Microarray ◽

Hypoxia Reoxygenation

Recent studies indicate that propofol may protect cells via suppressing autophagic cell death caused by excessive reactive oxygen species induced by hypoxia reoxygenation (H/R). It is established that gene expression patterns including autophagy-related genes changed significantly during the process of H/R in the presence or absence of propofol posthypoxia treatment (P-PostH). The reasons for such differences, however, remain largely unknown. MicroRNAs provide a novel mechanism for gene regulation. In the present study, we systematically analyzed the alterations in microRNA expression using human umbilical vein endothelial cells (HUVECs) subjected to H/R in the presence or absence of posthypoxic propofol treatment. Genome-wide profiling of microRNAs was then conducted using microRNA microarray. Fourteen miRNAs are differentially expressed and six of them were validated by the quantitative real-time PCR (Q-PCR) of which three were substantially increased, whereas one was decreased. To gain an unbiased global perspective on subsequent regulation by altered miRNAs, predicted targets of ten miRNAs were analyzed using the Gene Ontology (GO) analysis to build signaling networks. Interestingly, six of the identified microRNAs are known to target autophagy-related genes. In conclusion, our results revealed that different miRNA expression patterns are induced by propofol posthypoxia treatment in H/R and the alterations in miRNA expression patterns are implicated in regulating distinctive autophagy-related gene expression.

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Functional specialization of human circulating CD16 and CD1c myeloid dendritic-cell subsets

Blood ◽

10.1182/blood-2006-08-038422 ◽

2007 ◽

Vol 109 (12) ◽

pp. 5371-5379 ◽

Cited By ~ 145

Author(s):

Diego Piccioli ◽

Simona Tavarini ◽

Erica Borgogni ◽

Veronica Steri ◽

Sandra Nuti ◽

...

Keyword(s):

Cell Function ◽

Umbilical Vein ◽

Type I Interferons ◽

Type I ◽

Colony Stimulating Factor ◽

Tnf Α ◽

Macrophage Colony ◽

Umbilical Vein Endothelial Cells ◽

Factor Α ◽

Stimulating Factor

Abstract Human blood contains 2 populations of dendritic cells (DCs): plasmacytoid and myeloid (mDC). mDCs are subdivided into 3 subsets using the surface markers CD16, CD1c, and BDCA-3. Their role as pathogen sentinels and adjuvant targets was tested by phenotypic and functional analysis. We show that mDC subsets are immature and express mRNA for most toll-like receptors (TLRs), except for TLR3 in CD16-mDCs. The most represented subsets, CD16- and CD1c-mDCs, are similarly responsive to all TLR agonists. Among 31 cytokines tested, both subsets produce CXCL8 (IL-8)/tumor necrosis factor-α (TNF-α)/IL-6/CCL3 (MIP-1α)/CCL4 (MIP-1β)/IL-1β. CXCL8 (IL-8) is the predominant cytokine produced by CD1c-mDCs on TLR engagement, whereas all other cytokines, particularly TNF-α, are secreted in 10-fold to 100-fold higher amounts by CD16-mDCs. CD16-mDCs cocultured with human umbilical vein endothelial cells induce a significantly higher production of CXCL10 (IP-10), granulocyte-macrophage colony-stimulating factor, and granulocyte colony-stimulating factor than CD1c-mDCs. In addition, interleukin-3 and type I interferons are stimuli specifically for DC maturation rather than cytokine secretion, whereas TNF-α is almost ineffective in inducing either function, suggesting a mechanism of T-cell–DC crosstalk and of rapid induction of antigen-presenting cell function during viral infection rather than inflammation. In conclusion, CD16-mDCs show strong proinflammatory activity, whereas CD1c-mDCs appear to be mainly inducers of chemotaxis.

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