The mechanism of selenium regulating the permeability of vascular endothelial cells through selenoprotein O.

Vascular diseases, a leading cause of death in human, are strongly associated with pathological damage to blood vessels. The selenoprotein (Sel) have been reported to play important roles in vascular disease. However, the role of SelO in vascular disease has not been conclusively investigated. The present experiment was to investigate the regulatory mechanism of the effect of SelO on the permeability of vascular endothelial. The H.E staining, FITC-Dextran staining, Dil-AC-LDL staining and FITC-WGA staining showed that vascular structure was damaged, and intercellular junctions were disrupted with selenium (Se)-deficient. Immunohistochemistry, qPCR and Western blot revealed decreased expression of the adhesion plaque proteins vinculin, talin and paxillin, decreased expression of the vascular connectivity effector molecules connexin, claudin-1 and E-cadherin and increased expression of JAM-A and N-cadherin, as well as decreased expression of the ZO-1 signaling pathways ZO-1, Rock, rhoGEF, cingulin and MLC-2. In a screening of 24 Sel present in mice, SelO showed the most pronounced changes in vascular tissues, and a possible association between SelO and vascular intercellular junction effectors was determined using IBM SPSS Statistics 25. Silencing of SelO, vascular endothelial intercellular junction adverse effects present. The regulatory relationship between SelO and vascular endothelial intercellular junctions was determined. The results showed that Se deficiency lead to increased vascular endothelial permeability and vascular tissue damage by decreasing SelO expression, suggesting a possible role for SelO in regulating vascular endothelial permeability.

A collaborative effect of solid-phase denitrification and algae on secondary effluent purification.

This study explored the collaborative effect on nutrients removal performance and microbial community in solid-phase denitrification based bacteria-algae symbiosis system. Three biodegradable carriers (apple wood, poplar wood and corncob) and two algae species (Chlorella vulgaris and Chlorella pyrenoidosa) were selected in these bacteria-algae symbiosis systems. Results demonstrated that corncob as the carrier exhibited the highest average removal efficiencies of total nitrogen (83.7%-85.1%) and phosphorus removal (38.1%-49.1%) in comparison with apple wood (65.8%-71.5%, 25.5%-32.7%) and poplar wood (42.5%-49.1%, 14.2%-20.7%), which was mainly attributed to the highest organics availability of corncob. The addition of Chlorella acquired approximately 3%-5% of promotion rates for nitrated removal among three biodegradable carriers, but only corncob reactor acquired significant promotions by 3%-11% for phosphorous removal. Metagenomics sequencing analysis further indicated that Proteobacteria was the largest phylum in all wood reactors (77.1%-93.3%) and corncob reactor without Chlorella (85.8%), while Chlorobi became the most dominant phylum instead of Proteobacteria (20.5%-41.3%) in the corncob with addition of Chlorella vulgaris (54.5%) and Chlorella pyrenoidosa (76.3%). Thus, the higher organics availability stimulated the growth of algae, and promoted the performance of bacteria-algae symbiosis system based biodegradable carriers.

Trefoil Factor 3 Inhibits Thyroid Cancer Cell Progression Related to IL-6/JAK/STAT3 Signaling Pathway.

OBJECTIVES: Abnormal expression of trefoil factor 3 (TFF3) in breast, stomach, and colon tumors may be related to the occurrence of tumors, suggesting its role in angiogenesis. In this study, the aim was to explore the role of TFF3 in thyroid cancer. METHODS: TFF3 expression analysis was performed via GEPIA and RT-PCR. To explore the effects of TFF3 on thyroid cancer cell motility, cell function assays were performed. Furthermore, GSEA pathway analysis and western blot were used to explore the mechanism by which TFF3 represses the progression of thyroid cancer cells. RESULTS: Here, we showed that low expression level of TFF3 in thyroid cancer is related to thyroid cancer nodal metastasis. The patients with low TFF3 expression showed worse disease-free survival than those with high level of TFF3. Underexpressed TFF3 increased cell motility and inhibited cell apoptosis. We found that the levels of IL-6, p-JAK2/JAK2, and pSTAT3/STAT3 were inhibited in the pcDNA-TFF3 group compared to the pcDNA-NC group and these factors were upregulated in the si-TFF3 group compared to the si-NC group in BCPAP and TPC-1 cells. CONCLUSION: TFF3 inhibits thyroid cancer cell progression related to IL-6/JAK/STAT3 signaling pathway.