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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE164700 | GEO | 2022/01/05

REPOSITORIES: GEO

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Effect of prenatal sulforaphane (SUL) on hyperoxia-induced lung injury in Nrf2+/+ and Nrf2-/- neonates

Project description:Results: Prenatal SUL altered baseline lung genes involved in organ/cell development and grow (e.g., Ibsp, Ctsk, Igfbp5) and ARE responses (e.g., Aldh3a1, Maff, Mafg) in Nrf2+/+ neonates and in cell morphogenesis and cell death and organismal injury/abnormality inhibition (e.g., Neat1, Nox4, Vegfa, Igfbp2, Trp53) in Nrf2-/- neonates. In hyperoxia-exposed lung, prenatal SULincreased organogenesis/development genes (e.g., Prss35, Cep128) and decreased inflammatory genes (H2-D1, Cd40, Lcn2, Cdh22) in Nrf2+/+ pups. In Nrf2-/- mice exposed to hyperoxia, prenatal SFN decreased hyperoxia-upregulated many immune and inflammatory response genes (e.g., Ccl9, Btla, Ncf4, Ltb, Selplg, Csf2rb) and upregulated many DNA repair/damage checkpoint genes (e.g., Uimc1, Neil3, Nbn, Smc4, Smc6). Conclusion: Overall, prenatal maternal SUL altered genes differentially in Nrf2+/+ and Nrf2-/- lungs. However, SUL-mediated transcriptome changes affected similar biological functions benificial to host defense and organ development in both strain. Compensatory differential lung transcriptome changes in Nrf2-/- neonates may resulted in the manifest protection of their severe hyperoxic lung injury.

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

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