Significant role of long non-coding RNA MALAT1 in deep vein thrombosis via the regulation of vascular endothelial cell physiology through the microRNA-383-5p/BCL2L11 axis.

Deep vein thrombosis (DVT) is a vascular disease. The long non-coding RNA (lncRNA), metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), is positively expressed in DVT tissues, and regulates the biological behavior of endothelial progenitor cells. Here, we explored whether MALAT1 affected the physiology of human vascular endothelial cells (HUVECs) and analyzed its underlying mechanism. To overexpress/silence the expression of MALAT1 in HUVECs, MALAT1-plasmid/MALAT1-small interfering RNA (siRNA) was used. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide and flow cytometry analyses were performed to observe the cell viability and apoptosis. Reverse transcription-quantitative polymerase chain reaction and western blotting were used to determine the apoptosis-related protein and gene expression levels. We used Starbase software to predict the associations among MALAT1, microRNA (miR)-383-5p, and BCL2-like 11 (BCL2L11). Luciferase reporter assay was used to validate their relationship. Compared to the control vector group, MALAT1-plasmid suppressed the viability and induced apoptosis of HUVECs, while improving Bcl-2-associated X protein (Bax) expression and decreasing Bcl-2 expression. There was an interaction between MALAT1 and miR-383-5p. Compared to the control siRNA group, MALAT1-siRNA increased the cell viability, reduced cell apoptosis, upregulated Bcl-2 expression, and suppressed Bax expression. These changes were reversed by the miR-383-5p inhibitor. Additionally, we verified that BCL2L11 is a target of miR-383-5p. miR-383-5p improved the cell proliferation, while decreasing cell apoptosis in HUVECs by targeting BCL2L11. Therefore, the lncRNA-MALAT1/miR-383-5p/BCL2L11 axis may be effective for DVT treatment.

Mechanism of periplakin on ovarian cancer cell phenotype and its influence on prognosis.

Background: The aim of this paper was to investigate the clinical significance of periplakin (PPL) expression in ovarian cancer (OV) tissues and to explore the influence and possible mechanism of PPL on OV apoptosis. Methods: PPL expression in OV tissues was detected by western blotting, and its correlation with the clinicopathological parameters and prognosis of OV patients was analyzed. The influence of PPL expression on the growth of OV cell lines was analyzed using the DepMap database. The biological function of PPL and related genes in tumors was studied using Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis based on The Cancer Genome Atlas (TCGA) database. PPL expression in OV cell lines was detected by quantitative reverse transcription-polymerase chain reaction (RT-qPCR). The expression of apoptosis-related proteins in each group after PPL knockdown was detected by western blotting. Results: PPL expression in OV tissues was higher than that in normal ovarian tissues (P<0.05). PPL messenger RNA (mRNA) expression was highest in the OV cell line CAOV-4 and lowest in the OV cell line CoC1. PPL expression was decreased in the si-PPL-1, si-PPL-2, and si-PPL-3 groups, with significant inhibition in the si-PPL-1 and si-PPL-3 groups. Compared to that in the si-NC group, the cell proliferation rate in the si-PPL-1 and si-PPL-3 groups was decreased, and the apoptosis rate was increased. The expression of active caspase 3 and BCL-2-associated X (BAX) was increased, while that of B-cell lymphoma 2 (BCL-2) was decreased. Conclusions: PPL was highly expressed in OV tissues and cell lines, and this was related to the prognosis of OV patients. PPL might promote cancers by inhibiting OV apoptosis and could be a potential target of therapy for OV.

Alterations of the gut microbiome of largemouth bronze gudgeon (Coreius guichenoti) suffering from furunculosis.

High-throughput sequencing was applied to compare the intestinal microbiota in largemouth bronze gudgeon either healthy or affected by furunculosis. Proteobacteria, Actinobacteria, Tenericutes, Firmicutes and Bacteroidetes were detected as the predominant bacterial phyla in the gut of both diseased and healthy fish. The abundance of Proteobacteria differed significantly between the two groups of fish, mainly due to the overwhelming prevalence of Aeromonas in the diseased fish (81% ± 17%), while the genus was unevenly spread among the apparently healthy fish (33% ± 33%). The bacterial diversity in the intestine of diseased fish was markedly lower than in healthy fish. Analysis revealed the significant dissimilarity between the gut microbiota of diseased and healthy fish. The bacterial profiles in the gut were further characterized with the 28 phylotypes that were shared by the two groups. In diseased fish, two shared OTUs (OTU0001 and OTU0013) were closely related to Aeromonas salmonicida, their total proportion exceeding 70% of the sequences in diseased fish, while averaging 5.2% ± 4.6% in the healthy fish. This result suggested the presence of healthy carriers of pathogenic A. salmonicida among the farmed fish, and the gut appeared as a probable infection source for furunculosis in largemouth bronze gudgeon.