A quantitative review of the effects of Se application on the reduction of Hg concentration in plant: a meta-analysis

Mercury (Hg) is a highly toxic heavy metal entering the human body through the food chain after absorption by plant. Exogenous selenium (Se) has been suggested as a potential solution to reduce Hg concentration in plants. However, the literature does not provide a consistent picture of the performance of Se on the accumulation of Hg in plant. To obtain a more conclusive answer on the interactions of Se and Hg, 1,193 data records were collected from 38 publications for this meta-analysis, and we tested the effects of different factors on Hg accumulation by meta-subgroup analysis and meta-regression model. The results highlighted a significant dose-dependent effect of Se/Hg molar ratio on the reduction of Hg concentration in plants, and the optimum condition for inhibiting Hg accumulation in plants is at a Se/Hg ratio of 1–3. Exogenous Se significantly reduced Hg concentrations in the overall plant species, rice grains, and non-rice species by 24.22%, 25.26%, and 28.04%, respectively. Both Se(IV) and Se(VI) significantly reduced Hg accumulation in plants, but Se(VI) had a stronger inhibiting effect than Se(IV). Se significantly decreased the BAFGrain in rice, which indicated that other physiological processes in rice may be involved in restricting uptake from soil to rice grain. Therefore, Se can effectively reduce Hg accumulation in rice grain, which provides a strategy for effectively alleviating the transfer of Hg to the human body through the food chain

VEGFR-3 signaling restrains the neuron-macrophage crosstalk during neurotropic viral infection

Summary: Upon recognizing danger signals produced by virally infected neurons, macrophages in the central nervous system (CNS) secrete multiple inflammatory cytokines to accelerate neuron apoptosis. The understanding is limited about which key effectors regulate macrophage-neuron crosstalk upon infection. We have used neurotropic-virus-infected murine models to identify that vascular endothelial growth factor receptor 3 (VEGFR-3) is upregulated in the CNS macrophages and that virally infected neurons secrete the ligand VEGF-C. When cultured with VEGF-C-containing supernatants from virally infected neurons, VEGFR-3+ macrophages suppress tumor necrosis factor α (TNF-α) secretion to reduce neuron apoptosis. Vegfr-3ΔLBD/ΔLBD (deletion of ligand-binding domain in myeloid cells) mice or mice treated with the VEGFR-3 kinase inhibitor exacerbate the severity of encephalitis, TNF-α production, and neuron apoptosis post Japanese encephalitis virus (JEV) infection. Activating VEGFR-3 or blocking TNF-α can reduce encephalitis and neuronal damage upon JEV infection. Altogether, we show that the inducible VEGF-C/VEGFR-3 module generates protective crosstalk between neurons and macrophages to alleviate CNS viral infection