N6-methyladenosine (m6A) is the most prevalent modification in eukaryotic mRNA and potential regulatory functions of m6A have been shown by mapping the RNA m6A modification landscape. m6A modification in active gene regulation manifests itself as altered methylation profiles. The number of reports regarding to the profiling of m6A modification and its potential role in the placenta of preeclampsia (PE) is small. In this work, placental samples were collected from PE and control patients. Expression of m6A-related genes was investigated using quantitative real-time PCR. MeRIP-seq and RNA-seq were performed to detect m6A methylation and mRNA expression profiles. Gene ontology (GO) functional and Kyoto encyclopedia of genes and genomes (KEGG) pathway analyses were also conducted to explore the modified genes and their clinical significance. Our findings show that METTL3 and METTL14 were up-regulated in PE. In total, 685 m6A peaks were differentially expressed as determined by MeRIP-seq. Altered peaks of m6A-modified transcripts were primarily associated with nitrogen compound metabolic process, positive regulation of vascular-associated smooth muscle cell migration, and endoplasmic reticulum organisation. The m6A hyper-methylated genes of Wnt/β-catenin signalling pathway, mTOR signalling pathway, and several cancer-related pathways may contribute to PE. We also verified that the significant increase of HSPA1A mRNA and protein expression was regulated by m6A modification, suggesting m6A plays a key role in the regulation of gene expression. Our data provide novel information regarding m6A modification alterations in PE and help our understanding of the pathogenesis of PE.
The clinical significance of hsa-mir-1247 and hsa-mir-1269a expression in ectopic pregnancy due to salpingitis was investigated. Eighty patients with ectopic pregnancy diagnosed by ultrasonography who were admitted to Jinan Maternity and Child Care Hospital from January 2012 to May 2012 were enrolled in this study. To the observation group were assigned 35 patients whose ectopic pregnancy was due to salpingitis. The remaining 45 patients whose ectopic pregnancy was due to reasons other than endometriosis were assigned to the control group. Moreover, 32 healthy pregnant women were enrolled in this study at the same time as the healthy control group. Compared with the healthy control group, hsa-mir-1247 and hsa-mir-1269a were downregulated and upregulated, respectively, in patients with ectopic pregnancy (P<0.05). The difference was even more marked in patients with ectopic pregnancy due to salpingitis (P<0.05). The expression levels of hsa-mir-1247 and hsa-mir-1269a were negatively correlated, and the correlation coefficient r and P-value was −0.667 and 0.006, respectively. Abnormal expression of hsa-mir-1247 and hsa-mir-1269a may be risk factors for ectopic pregnancy. Abnormal expression of hsa-mir-1247 and hsa-mir-1269a found in patients with ectopic pregnancy due to salpingitis may be used as biomarkers of ectopic pregnancy.
Changes of micro-ribonucleic acid-182 (miR-182) level in cases of intrauterine infection were investigated to explore the association between miR-182 level change and brain injury in premature infants. A total of 257 preterm infants born in obstetrics department of Jinan Maternity and Child Care Hospital from February 2015 to February 2017 were enrolled in this study. These preterm infants were divided into infected group (n=113) and uninfected group (n=144) based on pathological diagnosis results. Quantitative polymerase chain reaction (qPCR) was employed to detect miR-182 level in amniotic fluid. Bregmatic sagittal and coronal plus lateral fontanel craniocerebral ultrasound, craniocerebral computed tomography (CT) and craniocerebral magnetic resonance imaging examinations were conducted in these preterm infants within one week after birth, and the results were recorded. The relationship between intrauterine infection and brain injury in premature infants was analyzed, and the association of miR-182 level with brain injury was explored. According to pathological diagnoses, brain injury was found in 61 of 113 infants in the infected group, with an incidence rate of 54.0%; and 28 of 144 infants in uninfected group, with an incidence rate of 19.4%; among them, 3 had placental infection caused by intrauterine infection in pregnant women, and all preterm infants had brain damage. Risk value of brain injury in premature infants due to intrauterine infection was hazard ratio (HR) = 2.2611, χ2=33.798, P<0.02. Infected group had a higher miR-182 level in comparison with uninfected group, and the difference in miR-182 level between infected group and uninfected group was statistically significant (P<0.05). Intrauterine infection can lead to an increase in miR-182 level; growth in miR-182 level is closely related to brain injury in premature infants.
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