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Human Papillomavirus (HPV) is considered as the major risk factor for the development and progression of cervical cancer. The high expression of HPV 16 E6 may be the causative factor for induction and maintenance of the transformed phenotype. These oncoproteins would interact with several intracellular proteins, such as eukaryotic translation initiation factor 5A-1 (eIF5A-1) that is essential for proliferation of eukaryotic cells. Our study explored the expression level of HPV 16 E6 and eIF5A-1 in human cervical squamous carcinoma samples and the adjacent non-cancerous cervix samples. Both C33a cells and SiHa cells transfected with a vector encoding HPV 16 E6 resulted in increase of eIF5A-1 expression level and enhancement of viability, migration and proliferation of these cells, furthermore, these effects in both C33a cells and SiHa cells could be abrogated by treatment with eIF5A-1 small-interfering RNA (siRNA) or the specific inhibitors ciclopirox (CPX) that was used to inhibit the function of eIF5A-1 via blocking the main enzymes deoxyhypusine hydroxylase (DOHH). Our results support that the silencing the eIF5A-1 gene or blocking the DOHH could induce the apoptosis of HPV 16 E6-infected cervical carcinoma cells. Thus might provide a new approach to preventing and treating cervical cancer., (Copyright © 2018. Published by Elsevier Inc.)

Circular RNAs (circRNAs) have recently been shown to exert their effects on multiple pathological processes by acting as microRNA (miRNA) sponges. However, the roles of circRNAs in gestational diabetes mellitus (GDM) are largely unknown. This study aimed to identify the circRNAs involved in GDM and predict their potential biological functions. We first performed next-generation sequencing (NGS) to generate unbiased placental villi circRNA expression profiles of GDM and normal controls. In total, 48,270 circRNAs from the placental villi of the two groups were sequenced. Of these, 227 circRNAs were significantly up-regulated and 255 circRNAs were significantly down-regulated. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) biological pathway analyses demonstrated that glycometabolism and lipometabolism processes, which are important in GDM development, were significantly enriched. Further analysis showed that most of the circRNAs harbored miRNA binding sites, and some were associated with GDM. These results showed that circRNAs are aberrantly expressed in the placental villi of GDM patients and play potential roles in the development of GDM., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Thy-1 nephritis (Thy-1 N), namely, anti-Thy-1 or anti-thymocyte serum (ATS) induced nephritis (ATSN), is a typical model of human mesangioproliferative glomerulonephritis. The pathologic changes of glomerular mesangial cells (GMCs) in Thy-1 N are complement-dependent, especially C5b-9 complexes, but the role of C5b-9 in the mechanism of Thy-1 N has not been defined. Because previous studies have demonstrated that sublytic C5b-9 can increase production of several inflammatory mediators from resident glomerular cells, we utilized the isolated human membrane-bound C5b-9 complexes to stimulate the cultured rat GMCs and examined whether the GMCs can also induce the synthesis of nitric oxide (NO) in vitro. Simultaneously, the effects of antiserum against rat C5b-9 and NG-monomethyl-L-arginine (L-NMMA, NO inhibitor), including interfering with the formation of C5b-9, reducing NO production and GMCs injury were observed. The results showed that sublytic C5b-9 can increase synthesis of inducible NO from the stimulated GMCs, and that the anti-C5b-9 antiserum can obviously inhibit the pathologic changes in Thy-1 N, while L-NMMA can decrease the GMCs damage although the effect is not so significant as that of the anti-C5b-9 antiserum. These findings indicate that the synthesis of NO by GMCs can be promoted by sublytic C5b-9, and that lesions of GMCs in rats with Thy-1 N are prevented by either inhibiting C5b-9 formation or NO elevation in advance. The pathologic changes of GMCs in Thy-1 N are indeed complement C5b-9-dependent, and the glomerular injury can be mediated in part through elevation of NO from the GMCs after the sublytic C5b-9 stimulation.