Early-life stress is a potent risk factor for development of psychiatric conditions such as depression. The underlying mechanisms remain poorly understood. Here, we used the early-life social isolation (ESI) model of early-life stress in rats to characterize development of depressive-like behavior, the role of microglia, levels of histone methylation, as well as expression of glutamate receptor subunits in the hippocampus. We found that depressive-like behavior was induced after ESI as determined by sucrose preference and forced swimming tests. Increased expression of microglial activation marker, Iba1, was observed in the hippocampus of the ESI group, while expression of the microglial CD200 receptor, which promotes microglial quiescence, significantly decreased. In addition, increased levels of proinflammatory cytokines, interleukin 1β (IL-1β), interleukin 6 (IL-6), and tumor necrosis factor-alpha (TNF-α) were observed in the hippocampus of the ESI group. Moreover, ESI increased levels of neuronal H3K9me2 (a repressive marker of transcription) and its associated "writer" enzymes, G9a and G9a-like protein, in the hippocampus. ESI also decreased expression of hippocampal NMDA receptor subunits, NR1, and AMPA receptor subunits, GluR1 and GluR2, which are involved in synaptic plasticity, but it did not affect expression of PSD95 and NR2B. Interestingly, treatment with minocycline to block microglial activation induced by ESI inhibited increases in hippocampal microglia and prevented ESI-induced depressive-like behavior as well as increases in IL-1β, IL-6, and TNF-α. Notably, minocycline also triggered downregulation of H3K9me2 expression and restored expression of NR1, GluR1, and GluR2. These results suggest that ESI induces depressive-like behavior, which may be mediated by microglial signaling.

Maintaining undifferentiated state and self-renewal ability of embryonic stem cells is a process that many genes and factors participate in. Using bioinformatics analyses and suppression subtractive hybridization we cloned a novel human gene related to the proliferation of human embryonic stem (hES) cells and its mouse homologue and identified them as being borealin. Our data demonstrated that borealin was highly expressed in undifferentiated ES cells, mouse pre-implantation embryos and the brain of 8.5-9.5 day post-coitum mouse embryos. Furthermore, following Borealin depletion by microinjecting anti-Borealin antibody into the zygotes the mouse embryos were arrested at the 2 or 4-cell stage and chromosomes could not correctly localize at the equator plane of the mitotic spindle and most cells had two or more nuclei. Taken together, these results indicate that Borealin plays a crucial role in the early mouse embryonic development.

Atherosclerosis (AS) is one of the most common cardiovascular system diseases which seriously affects public health in modern society. Finding potential biomarkers in the complicated pathological progression of AS is of great significance for the prevention and treatment of AS. Studies have shown that long noncoding RNAs (lncRNAs) can be widely involved in the regulation of many physiological processes, and have important roles in different stages of AS formation. LncRNAs can be secreted into the circulatory system through exosomes, microvesicles, and apoptotic bodies. Recently, increasing studies have been focused on the relationships between circulating lncRNAs and AS development. The lncRNAs in circulating blood are expected to be new non-invasive diagnostic markers for monitoring the progression of AS. We briefly reviewed the previously reported lncRNA transcripts which related to AS development and detectable in circulating blood, including ANRIL, SENCR, CoroMarker, LIPCAR, HIF1α-AS1, LncRNA H19, APPAT, KCNQ1OT1, LncPPARδ, LincRNA-p21, MALAT1, MIAT, and UCA1. Further researches and a definition of atherosclerosis-associated circulating lncRNA (ASCLncRNA) were also discussed.

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