Abstract：
:Fetal overexposure to active glucocorticoid (GC) is the major cause for fetal growth restriction (FGR). This study investigated the influences of cadmium (Cd) exposure on active GC and its mechanism in placental trophoblasts. Pregnant mice were exposed to CdCl2 (4.5 mg/kg, i.p.). Human JEG-3 cells were treated with CdCl2 (0-20 μM). Prenatal Cd exposure significantly increased active GC level in amniotic fluid and placenta. Similarly, Cd treatment also elevated active GC level in medium. Expectedly, the expression of 11β-HSD2 protein was markedly downregulated in Cd-exposed placental trophoblasts. We further found that Cd activated the PERK/p-eIF2α signaling pathway in placental trophoblasts. Mechanistically, PERK siRNA pretreatment completely blocked PERK/p-eIF2α signaling, and thereby restoring Cd-downregulated 11β-HSD2 protein expression in human placental trophoblasts. We further found that N-acetylcysteine, a well-known antioxidant, obviously reversed Cd-downregulated 11β-HSD2 protein expression by inhibiting p-PERK/p-eIF2α signaling in placental trophoblasts. Overall, our data suggest that Cd activates the PERK/p-eIF2α signaling, down-regulates the protein expression of 11β-HSD2, and thereby elevating active GC level in placental trophoblast.
journal_name
Chemospherejournal_title
Chemosphereauthors
Shi XT,Zhu HL,Xiong YW,Liu WB,Zhou GX,Cao XL,Yi SJ,Dai LM,Zhang C,Gao L,Xu DX,Wang Hdoi
10.1016/j.chemosphere.2020.126785subject
Has Abstractpub_date
2020-09-01 00:00:00pages
126785eissn
0045-6535issn
1879-1298pii
S0045-6535(20)30978-4journal_volume
254pub_type
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