Articles written in Journal of Biosciences
Volume 35 Issue 1 March 2010 pp 63-71
Early-life endocrine intervention may programme hippocampal glucocorticoid receptor (GR) expression and cause psychiatric disorders in later life. Glucagon-like peptide-1 (GLP-1) has been implicated in the regulation of neuroendocrine and behavioural responses, but it is yet to be determined whether and how neonatal GLP-1 overexpression may modify hippocampal GR expression and thus programme adolescent behaviour in rats. Two-dayold pups were injected intramuscularly with vacant plasmid (VP) or plasmid DNA encoding secretory GLP-1 (GP). Anxiety-related behaviour was assessed in the elevated plus maze (EPM) test at 8 weeks of age. Plasma corticosterone levels were measured with enzyme immunoassay (EIA). Protein and mRNA levels were determined by western blot and real-time polymerase chain reaction (PCR), respectively. The DNA methylation status of the GR exon 17 promoter was determined by bisulphate sequencing PCR (BSP). GP rats exhibited anxiolytic behaviour compared with their VP counterparts. Hippocampal GLP-1 receptor (GLP-1R) and GR mRNA expression were significantly elevated in GP rats without a significant difference in plasma corticosterone. Significant reduction in DNA methyltransferase 1 (DNMT1) expression was observed in GP rats disconnected with alterations in DNA methylation of the GR exon 17 promoter. Nevertheless, mRNA expression of nerve growth factor-inducible protein A (NGFI-A) was significantly elevated in GP rats. These results suggest that neonatal intramuscular injection of plasmid DNA encoding GLP-1 affects anxiety behaviour in adolescent rats, probably through NGFI-A-activated upregulation of hippocampal GR expression.
Volume 46 All articles Published: 1 July 2021 Article ID 0065 Article
N-3-(oxododecanoyl)-L-homoserine lactone (3-O-C12-HSL), a small bacterial signaling molecule secreted byPseudomonas aeruginosa (P. aeruginosa), can block dendritic cell (DC) maturation and participate in immuneescape, but the underlying mechanism is unclear. We speculate that regulation of DC maturation and functionby lncRNAs may be the mechanism by which 3-O-C12-HSL inhibits the immune response. We found that3-O-C12-HSL increased the expression level of the lncRNA NRIR, impeding monocyte-derived dendritic cell(Mo-DC) maturation. In addition, we observed the effect of NRIR on the expression of CD40, CD80, HLA-DRand IL-6. NRIR overexpression significantly reduced the expression of Mo-DC surface markers, while 3-OC12-HSL did not significantly reduce the expression of Mo-DC surface markers after NRIR knockdown.These results indicate that 3-O-C12-HSL indeed affects the differentiation and maturation of Mo-DCs throughNRIR. IL-6 stimulates T cell proliferation and activation, and we found that high NRIR expression reduced IL-6 levels. However, under NRIR knockdown, 3-O-C12-HSL did not decrease IL-6 expression, suggesting that3-O-C12-HSL may affect T cell activation through NRIR. This study is the first to elucidate the important roleof a lncRNA in the mechanism of 3-O-C12-HSL activity. It also provides new ideas regarding P. aeruginosainfection pathogenesis.
Volume 46, 2020
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