Mitochondrial DNA-Activated cGAS-STING Signaling in Environmental Dry Eye.

Purpose: The cGAS-STING pathway has been shown to be an important mediator of inflammation. There is emerging evidence of the importance of this signaling cascade in a variety of inflammatory diseases settings. Here, we present evidence that the mitochondrial DNA (mtDNA) damage-mediated cGAS-STING pathway plays an important role in the induction of inflammation in environmental dry eye (DE).

Single-cell landscape reveals the epithelial cell-centric pro-inflammatory immune microenvironment in dry eye development.

Dry eye disease (DED) is a prevalent chronic eye disease characterized by an aberrant inflammatory response in ocular surface mucosa. The immunological alterations underlying DED remain largely unknown. In this study, we employed single-cell transcriptome sequencing of conjunctival tissue from environment-induced DED mice to investigate multicellular ecosystem and functional changes at different DED stages.

Epigenetic Activation of Circadian Clock Genes Elicits Inflammation in Experimental Murine Dry Eye.

Purpose: To explore whether circadian clock genes contribute to elicit inflammation in experimental dry eye (EDE).

Methods: RNA sequencing analyzed mRNA expression patterns in EDE model. RT-qPCR and/or Western blot determined the expression of inflammatory factors and circadian genes during EDE.

Proteomic identification of sperm from mice exposed to sodium fluoride.

Fluoride is a widespread environmental pollutant which can induce low sperm quality and fertilizing ability. However, effect of fluoride on proteomic changes of sperm is unknown. In this study, two-dimensional electrophoresis (2DE) and mass spectrometry (MS) were used to investigate the differently expressed proteins of sperm from mice exposed to fluoride.

Paternal bisphenol a diet changes prefrontal cortex proteome and provokes behavioral dysfunction in male offspring.

Relatively little attention has been given paternal effects on next generation. Given that Bisphenol A (BPA), a ubiquitous compound in maternal diet, may disrupt brain development and behavior, we hypothesized that paternal BPA diet (PBD) could affect offspring development. Prefrontal cortex (PFC), a vital brain region, is involved in emotion and social behavior.

Chronic fluoride exposure-induced testicular toxicity is associated with inflammatory response in mice.

Previous studies have indicated that fluoride (F) can affect testicular toxicity in humans and rodents. However, the mechanism underlying F-induced testicular toxicity is not well understood. This study was conducted to evaluate the sperm quality, testicular histomorphology and inflammatory response in mice followed F exposure.

Fluoride exposure changed the structure and the expressions of reproductive related genes in the hypothalamus-pituitary-testicular axis of male mice.

Numerous studies have shown that fluoride exposure adversely affected the male reproductive function, while the molecular mechanism is not clear. The present study was to investigate the effects of fluoride exposure (60 days) on the expressions of reproductive related genes, serum sex hormone levels and structures of the hypothalamus-pituitary-testicular axis (HPTA), which plays a vital role in regulating the spermatogenesis in male mice. In this study, 48 male mice were administrated with 0, 25, 50, and 100 mg/L NaF through drinking water.

Maternal bisphenol a diet induces anxiety-like behavior in female juvenile with neuroimmune activation.

Maternal Bisphenol A (BPA) diet triggers anxiety in rodents, but the underlying mechanism is still unclear. Accumulating epidemiological and experimental data have demonstrated that the anxiety is associated with aberrant neuroimmune response. In this study, we found that maternal BPA diet (MBD) exacerbated anxiety-like behavior in female juvenile mice, and the molecular evidence further showed that this behavioral phenotype was connected to the neuroimmune activation, such as elevated tumor necrosis factor alpha (TNF-α) and interleukin (IL)-6 levels in prefrontal cortex (PFC) rather than in peripheral blood, which indicated that neuroimmune response might be ascribed to neuroglial activation because activated neuroglia cells could secrete proinflammatory cytokines.

Pubertal exposure to Bisphenol A increases anxiety-like behavior and decreases acetylcholinesterase activity of hippocampus in adult male mice.

The negative effects of Bisphenol A (BPA) on neurodevelopment and behaviors have been well established. Acetylcholinesterase (AChE) is a regulatory enzyme which is involved in anxiety-like behavior. This study investigated behavioral phenotypes and AChE activity in male mice following BPA exposure during puberty.