Placenta-Specific Transcripts Containing Androgen Response Elements Are Altered In Silico by Male Growth Outcomes.
Ashley S MeakinMelanie D SmithJanna L MorrisonClaire T RobertsMartha LappasStacey J ElleryOlivia J HollandAnthony V PerkinsSharon A McCrackenVicki FlenadyVicki L CliftonPublished in: International journal of molecular sciences (2024)
A birthweight centile (BWC) below the 25th is associated with an elevated risk of adverse perinatal outcomes, particularly among males. This male vulnerability may stem from alterations in placenta-specific androgen signalling, a signalling axis that involves the androgen receptor (AR)-mediated regulation of target genes containing androgen response elements (AREs). In this study, we examined global and ARE-specific transcriptomic signatures in term male placentae (≥37 weeks of gestation) across BWC subcategories (<10th, 10th-30th, >30th) using RNA-seq and gene set enrichment analysis. ARE-containing transcripts in placentae with BWCs below the 10th percentile were upregulated compared to those in the 10th-30th and >30th percentiles, which coincided with the enrichment of gene sets related to hypoxia and the suppression of gene sets associated with mitochondrial function. In the absence of ARE-containing transcripts in silico, <10th and 10th-30th BWC subcategory placentae upregulated gene sets involved in vasculature development, immune function, and cell adhesion when compared to those in the >30th BWC subcategory. Collectively, our in silico findings suggest that changes in the expression of ARE-containing transcripts in male placentae may contribute to impaired placental vasculature and therefore result in reduced fetal growth outcomes.
Keyphrases
- genome wide
- rna seq
- genome wide identification
- copy number
- single cell
- gestational age
- molecular docking
- cell adhesion
- preterm infants
- dna methylation
- genome wide analysis
- pregnant women
- gene expression
- climate change
- type diabetes
- adipose tissue
- endothelial cells
- skeletal muscle
- metabolic syndrome
- emergency department
- insulin resistance