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The coparenting subsystem is important for the psychosocial development of young children. In this article, we used cross-lagged structural equation modeling to assess the bidirectional relations between unmarried parents’ cooperative coparenting and their children’s behavioral problems. Using a subsample of 788 dyads of poor, unmarried parents and their children from the Fragile Families and Child Wellbeing data, we examined trends in coparenting and behavioral problems over time (in children ages 1, 3, 5, and 9 years) and the reciprocal effects between these 2 variables. All pathways from coparenting at 1 time point to the children’s behavioral problems at the following time point were significant, indicating that cooperative coparenting at earlier time points is likely to result in fewer behavioral problems in children at later time points. A cross-lagged path from behavioral problems to coparenting in the preschool years was also statistically significant. Implications for interventions and next steps for further research are discussed.

MicroRNAs (miRNAs) have been proven to have important effects on the proliferation and metastasis of multiple cancers, including hepatocellular carcinoma (HCC). In the present study, our aim was to explore the biological function of miR-106b in HCC cell proliferation and metastasis. qPCR analysis showed that miR-106b was expressed at higher levels, while disabled homolog 2 (DAB2) was expressed at lower levels in HCC tissues and cells. Moreover, the aberrant miR-106b expression in HCC affected the cell proliferative and migratory ability by MTT and Transwell assay. DAB2 was identified as a specific target of miR-106b in HCC by luciferase reporter assay and regression analysis showed a negative correlation between DAB2 and miR-106b expression. In addition, DAB2 may attenuate the miR-106b promotion effect on HCC cell proliferation and migration. In short, miR-106b may promote HCC cell proliferation and migration by targeting DAB2.

Background Macrophage polarization and microRNA play crucial roles in the development of atherosclerosis (AS). The M1 macrophage phenotype contributes to the formation of plaques, while the M2 macrophage phenotype resolves inflammation and promotes tissue repair. MiR-126 has been found to play a role in regulating macrophage polarization in the context of AS. However, the exact mechanism of miR-126 requires further research. Methods The foam cell model was established by stimulating THP-1 with oxidized low-density lipoprotein (ox-LDL). We transfected foam cells with miR-126 mimic and its negative control. The transfection of miR-126 was implemented by riboFECT CP transfection kit. The levels of miR-126 and M1/M2 associated genes in foam cells were quantified using reverse transcription-quantitative PCR (RT-qPCR). Additionally, the expressions of CD86+ and CD206+ cells in foam cells were determined by flow cytometry. Western blotting and RT-qPCR were used to determine the protein and mRNA levels of the vascular endothelial growth factor A (VEGFA) and the transcriptional regulator Krüppel-like factor 4 (KLF4), respectively. Additionally, we detected endothelial cell migration after co-culturing endothelial cells and macrophages. MG-132 was used to indirectly activate the expression of VEGFA, and the expression of KLF4 was also evaluated. Results The activation of apoptosis and production of foam cells were boosted by the addition of ox-LDL. We transfected foam cells with miR-126 mimic and its negative control and observed that miR-126 greatly suppressed foam cell development and inhibited phagocytosis. Moreover, it caused pro-inflammatory M1 macrophages to switch to the anti-inflammatory M2 phenotype. This was reflected by the increase in anti-inflammatory gene expression and the decrease in pro-inflammatory gene expression. Additionally, miR-126 dramatically decreased the expressions of VEGFA and KLF4. The protein-protein interaction network analysis showed a significantly high correlation between miR-126, VEGFA, and KLF4. MiR-126 may also promote EC migration by activating macrophage PPAR γ expression and effectively suppressing macrophage inflammation. MG-132 indirectly activated the expression of VEGFA, and the expression of KLF4 also significantly increased, which indicates a direct or indirect relationship between VEGFA and KLF4. Conclusion Our study shows that miR-126 can reverse ox-LDL-mediated phagocytosis and apoptosis in macrophages. Consequently, the potential role of miR-126 was manifested in regulating macrophage function and promoting vascular endothelial migration.

Investigations on the bidirectional relationships between parenting stress and child behavior problems are important to inform intervention strategies; however, prior research has provided inconsistent findings. Using a national sample of multi-stressed single-mother families from the Fragile Families and Child Wellbeing study, the present study examined the bidirectional relationships between maternal parenting stress and children's behavioral problems spanning from early childhood through adolescence at the child's ages 3, 5, 9, and 15. Reciprocal transactions were found between parenting stress and behavior problems in early childhood between the ages 3 and 5. From age 5 to age 15, our findings also suggest that children's behavior problems at an earlier time point predict mothers' parenting stress at a later time point. Unexpectedly, the lagged effects of parenting stress on child behavior problems in school ages were not significant in our sampled data. Early childhood interventions should address mitigating both parenting stress and their toddlers' behavior problems. During middle childhood and adolescence, interventions to directly address children's behavior problems are critical both to the well-being of mothers and to assist in the reduction in levels of behavior problems.