Pre-eclampsia is thought to be a systemic disease of maternal endothelial cell dysfunctions. miRNAs regulate various basic biological functions in cells, including stem cells. Mesenchymal stem cells exist in almost all tissues and are the key cellular source for tissue repair and regeneration. Our aims are to investigate whether miRNAs regulate MSCs in fetal-maternal interfaces to influence the pathogenesis of pre-eclampsia. The differential expression of miRNAs in decidua-derived mesenchymal stem cells of all patients with severe pre-eclampsia (n = 20) and normal groups (n = 20) was first screened by microarray analysis and validated by quantitative real-time PCR analysis. The integrated bioinformatics analysis showed that miR-16 showed the highest number of connections in the miRNA GO network and the miRNA gene network. Moreover, over-expressed miR-16 inhibited the proliferation and migration of decidua-derived mesenchymal stem cells and induced cell-cycle arrest by targeting cyclin E1. Interestingly, over-expression of miR-16 by decidua-derived mesenchymal stem cells reduced the ability of human umbilical vein endothelial cells to form blood vessels and reduced the migration of trophoblast cells. Furthermore, decidua-derived mesenchymal stem cell-expressed endothelial growth factor VEGF-A was involved in migration of trophoblast cells and human umbilical vein endothelial cells as well as tube and network formation. Importantly, the levels of cyclin E1 and VEGF-A were negatively correlated with the level of miR-16 expression in decidua-derived mesenchymal stem cells from the patients with severe pre-eclampsia. Together, these data suggest that the alteration of miR-16 expression in decidua-derived mesenchymal stem cells may be involved in the development of pre-eclampsia.Abbreviations CCNE1/D1, cyclin E1 and D1; CDK2/6, cyclin-dependent kinase 2 and 6; dMSCs, decidua-derived MSCs; HUVEC, human umbilical vein endothelial cells; MSCs, mesenchymal stem cells; pre-miR-16, miR-16 precursor; sPE, severe pre-eclampsia; VEGF-A, endothelial growth factor.

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Mesenchymal stem cells (MSCs) play an important role in regulating angiogenesis and immune balance. The abnormal MSCs in proliferation and function were reported at maternal fetal interface in patients with pre-eclampsia (PE). Long non-coding RNA MALAT1 was known to regulate the function of trophoblast cells. However, it is not clear whether MALAT1 regulates MSCs to be related to PE. In the present study, we found that the expression of MALAT1 was significantly reduced in both umbilical cord tissues and MSCs in patients with severe PE. MALAT1 did not affect the phenotype and differentiation of MSCs. Of note, transfection with MALAT1 plasmid into MSCs drove the cell cycle into G2/M phase and inhibited cell apoptosis. The supernatants from MALAT1-overexpressed MSCs promoted the migration of MSCs, invasion of HTR-8/SVneo and tube formation of HUVEC, while si-MALAT1 had the opposite effects. Moreover, we found that MALAT1-induced VEGF mediated these effects of MALAT1 on MSCs. Furthermore, we found that MALAT1-overexpressed MSCs promoted M2 macrophage polarization and this effect was mediated by MALAT1-induced IDO expression, suggesting that MALAT1 may enhance the immunosuppressive properties of MSCs in vivo. In addition, we also investigated the factors that inhibit MALAT1 expression in PE and found that peroxide was a cause for MALAT1 downregulation. Taken together, our data demonstrate that MALAT1 is an important endogenous regulator in the proliferation, angiogenesis, and immunosuppressive properties of MSCs, suggesting it may be involved in the pathogenesis of PE. J. Cell. Biochem. 118: 2780-2791, 2017. © 2017 Wiley Periodicals, Inc.

The microstructure and phase composition of an AlCoCrFeNi high-entropy alloy (HEA) were studied in as-cast (AlCoCrFeNi-AC, AC represents as-cast) and homogenized (AlCoCrFeNi-HP, HP signifies hot isostatic pressed and homogenized) conditions. The AlCoCrFeNi-AC ally has a dendritrical structure in the consisting primarily of a nano-lamellar mixture of A2 [disorder body-centered-cubic (BCC)] and B2 (ordered BCC) phases, formed by an eutectic reaction. The homogenization heat treatment, consisting of hot isostatic pressed for 1 hour at 1,100 °C, 207 MPa and annealing at 1,150 °C for 50 hours, resulted in an increase in the volume fraction of the A1 phase and formation of a Sigma () phase. Tensile properties in ascast and homogenized conditions are reported at 700 °C. The ultimate tensile strength was virtually unaffected by heat treatment, and was 396 ± 4 MPa at 700 °C. However, 2 homogenization produced a noticeable increase in ductility. The AlCoCrFeNi-AC alloy showed a tensile elongation of only 1.0 %, while after the heat-treatment, the elongation of AlCoCrFeNi-HP was 11.7 %. Thermodynamic modeling of non-equilibrium and equilibrium phase diagrams for the AlCoCrFeNi HEA gave good agreement with the experimental observations of the phase contents in the AlCoCrFeNi-AC and AlCoCrFeNi-HP. The reasons for the improvement of ductility after the heat treatment and the crack initiation subjected to tensile loading were discussed.

Significance Thin endometrium is the most common reason for uterine infertility and refractory gynecological diseases due to its complexity in pathogenesis and adverse pregnancy outcomes. Here, we profile cells from normal and thin endometrium at single-cell resolution to investigate the sophisticated alterations in the local microenvironment that occur in thin endometrium. Increased cellular senescence, collagen overdeposition, and significant down-regulation of gene expression related to cell proliferation are observed and confirmed. Moreover, we demonstrate aberrant activation of the SEMA3 pathway accompanied by dampened EGF, PTN, and TWEAK signaling pathways in thin endometrium. These findings aid in understanding the mechanisms of thin endometrium and provide new tools to rejuvenate the atrophic endometrium for female fertility preservation and successful pregnancy.