PubMed · 8242135
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G Zon. 1993. Oligonucleoside phosphorothioates.. https://doi.org/10.1385/0-89603-281-7%3A165
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To test our hypothesis that proatherogenic lysophosphatidylcholine (LPC) upregulates trained immunity pathways (TIPs) in human aortic endothelial cells (HAECs), we conducted an intensive analyses on our RNA-Seq data and histone 3 lysine 14 acetylation (H3K14ac)-CHIP-Seq data, both performed on HAEC treated with LPC. Our analysis revealed that: 1) LPC induces upregulation of three TIPs including glycolysis enzymes (GE), mevalonate enzymes (ME), and acetyl-CoA generating enzymes (ACE); 2) LPC induces upregulation of 29% of 31 histone acetyltransferases, three of which acetylate H3K14; 3) LPC induces H3K14 acetylation (H3K14ac) in the genomic DNA that encodes LPC-induced TIP genes (79%) in comparison to that of in LPC-induced effector genes (43%) including ICAM-1; 4) TIP pathways are significantly different from that of EC activation effectors including adhesion molecule ICAM-1; 5) reactive oxygen species generating enzyme NOX2 deficiency decreases, but antioxidant transcription factor Nrf2 deficiency increases, the expressions of a few TIP genes and EC activation effector genes; and 6) LPC induced TIP genes(81%) favor inter-chromosomal long-range interactions (CLRI, trans-chromatin interaction) while LPC induced effector genes (65%) favor intra-chromosomal CLRIs (cis-chromatin interaction). Our findings demonstrated that proatherogenic lipids upregulate TIPs in HAECs, which are a new category of qualification markers for chronic disease risk factors and conditional DAMPs and potential mechanisms for acute inflammation transition to chronic ones. These novel insights may lead to identifications of new cardiovascular risk factors in upregulating TIPs in cardiovascular cells and novel therapeutic targets for the treatment of metabolic cardiovascular diseases, inflammation, and cancers. (total words: 245).
Nucleosomes prevent the recognition of TATA promoter elements by the basal transcriptional machinery in the absence of induction. However, while Saccharomyces cerevisiae histones H3 and H4 contain N-terminal regions involved in the activation and repression of GAL1 and in the expression of heterochromatin-like regions, the sequences involved in repressing basal transcription have not yet been identified. Here, we describe the mapping of new N-terminal domains, in all four core histones (H2A, H2B, H3 and H4), required for the repression of basal, uninduced transcription. Basal transcription was monitored by the use of a GAL1 promoter-URA3 reporter construct whose uninduced activity can be detected through cellular sensitivity to the drug, 5-fluoroorotic acid. We have found for each histone that the N-terminal sequences repressing basal activity are in a short region adjacent to the structured alpha-helical core. Analysis of minichromosome DNA topology demonstrates that the basal domains are required for the proper folding of DNA around the chromosomal particle. Deletion of the basal domain at each histone significantly decreases plasmid superhelical density, which probably reflects a release of DNA from the constraints of the nucleosome into the linker region. This provides a means by which basal factors may recognize otherwise repressed regulatory elements.
Sugar chain types were classified on the basis of reducing end di- and trisaccharide structures. Sugar chains liberated from glycoproteins by the hydrazinolysis-N-acetylation method were pyridylaminated, and pyridylamino (PA-) sugar chains were purified by HPLC. The PA-sugar chains thus purified were partially hydrolyzed with 1 M trifluoroacetic acid. The acid hydrolysis conditions were investigated with the object of obtaining PA-di- and trisaccharides with high yields for different types of PA-sugar chains. The acid hydrolysates were separated by size-fractionation HPLC into PA-mono-, PA-di-, and PA-trisaccharides, and each fraction was analyzed by reversed-phase HPLC. The structures were then identified by comparing the HPLC elution positions with those of authentic PA-oligosaccharides derived from N-linked sugar chains and 12 types of O-linked sugar chains.