Analysis of differential expression of hypoxia-inducible microRNA-210 gene targets in mild and severe preeclamptic patients

Preeclampsia (PE) is a multi-system disorder that is specific to human pregnancy. Inadequate oxygenation of uterus and placenta is considered as one of the leading causes for the disease. MicroRNA-210(miR-210) is one of the prime molecules that has emerged in response to hypoxia. The objective of this study was to determine miR-210 expression patterns in plasma from severe PE and mild PE patients, and how that affects the expression of miR-210 target genes. The expression levels of miR-210 were validated using reverse transcription-quantitative PCR in plasma of severe PE (15) and mild PE (15) patients in comparison to controls subjects (15) with normal pregnancy. Then, the association between miR-210 and its downstream genes was validated by using human miR-210 targets RT2 profiler PCR Array. Both the categories (mild and severe) showed significantly high miR-210 expression levels. Also out of the 84 hypoxia miR-210 associated genes screened using mRNA, 18 genes were found to be differentially expressed in severe PE whereas 16 genes in mild PE cases with varying magnitude. All the genes in both the PE groups were found downregulated in comparison to controls. These downregulated genes expressed in both the cases were shown to be participating in immunosuppression, apoptosis, cell growth, signaling, angiogenesis, DNA repair. This study provides novel data on the genes that work downstream of miR-210 and how dysregulated expression of miR-210 can affect their expression and in turn functioning which can be associated with PE risk and severity. This study is the very first to determine the effect of miR-210 expression levels on associated genes in plasma samples

Data from: Analysis of VEGFA variants and changes in VEGF levels underscores the contribution of VEGF to polycystic ovary syndrome

Background. Vascular endothelial growth factor (VEGF) contributes to the pathogenesis of polycystic ovary syndrome (PCOS), and genetic variations in VEGFA gene were suggested to contribute to VEGF secretion and PCOS. Aim. To evaluate the association of altered VEGF levels, stemming from the presence of specific VEGFA variants, with altered risk of PCOS. Subjects and Methods. Retrospective case-control study, performed between 2012-2015. Study subjects comprised 382 women with PCOS, and 393 control subjects. ELISA measured VEGF levels; genotyping of VEGFA variants was done by allelic exclusion. Results. Among the 12 tested VEGFA SNPs, minor allele frequency of only rs3025020 was significantly higher in PCOS cases than control women. Increased and reduced PCOS risk was seen with rs3025020 and rs2010963 genotypes, respectively. Increases and reduction in VEGF levels were associated with rs3025020 and rs2010963, respectively. Increased fasting insulin and HOMA-IR, and bioactive testosterone were linked with rs3025020, while carriage of rs2010963 was linked with reduction in fasting insulin, and free and bioactive testosterone. Of the 12 VEGFA variants, 9 were in LD, thus allowing construction of 9-locus haplotypes. Increased frequency of CAACAGCGA haplotype was seen in PCOS cases, after controlling for BMI, free and bioactive testosterone, SHBG, free insulin and HOMA-IR. Conclusion. This study confirms the contribution of altered VEGF secretion, resulting from genetic variation in VEGFA gene into the pathogenesis of PCOS. This supports a role for VEGF as PCOS candidate locus

Almawi PLoS One data

VEGF SNP analysis in 382 women with PCOS and 393 control women. Genotyping was done by real-time PCR (ABI StepOne Plus)