Effect of prenatal sulforaphane (SUL) on Nrf2+/+ and Nrf2-/- placenta

Results: In Nrf2+/+ placenta, genes involved in estrogen receptor signaling and reproductive system development (e.f., Med subfamily, Igf1r, Ncor2), vasculature and embryonic development (e.g., Adamdec1, Pdgfrb, Col8a2, Sema3g, Krt5, Lce1a1), and inhibition of prenatal death and cell morbidity (e.g., Dnmt3a, Col4a2) were regulated by SFN. Multiple granzyme isozymes (Gzmd, Gzmg, Gzmf, Gzmc) and oxidoreduction genes (e.g., Gstt1, Gstt2, Prdx5, Hao3, Hsd17b10, Pecr) were suppressed in Nrf2+/+ placenta treated with SFN. SFN-altered transcriptome changes in Nrf2-/- placenta were predicted to inhibit prenatal death via regulation of genes including Igf2r, Tgfb2, Arid5b, and Il6st and to activate angiogenesis and cell growth by alteration of genes such as Timp3, Kdr, and Il6ra. Conclusion: Overall transcriptome changes indicated reduced cytotoxicity and activated feto-placenta barrier functions in both Nrf2+/+ and Nrf2-/- mice. PARALLEL study design with 12 samples comparing 48 groups of prenatal treatment (PBS, SUL) and gene (Nrf2-WT, Nrf2-KO). (2 groups of Nrf2-WT; PBS, SUL), (2 groups of Nrf2-KO; PBS, SUL) Biological replicates: 3 per group