TY  - JOUR
U1  - Zeitschriftenartikel, wissenschaftlich - begutachtet (reviewed)
A1  - Sunny, Donna Elizabeth
A1  - Triller, Paul
A1  - Brandt, Stephan A.
A1  - Schmidt, Sein H.
T1  - Fetal zone steroids and estrogen show sex specific effects on oligodendrocyte precursor cells in response to oxidative damage.
JF  - International Journal of Molecular Sciences
N2  - Oxygen causes white matter damage in preterm infants and male sex is a major risk factor
for poor neurological outcome, which speculates the role of steroid hormones in sex-based differences.
Preterm birth is accompanied by a drop in 17β-estradiol (E2) and progesterone along with increased
levels of fetal zone steroids (FZS). We performed a sex-based analysis on the FZS concentration
differences in urine samples collected from preterm and term infants. We show that, in preterm
urine samples, the total concentration of FZS, and in particular the 16α-OH-DHEA concentration, is
significantly higher in ill female infants as compared to males. Since we previously identified Nup133
as a novel target protein affected by hyperoxia, here we studied the effect of FZS, allopregnanolone
(Allo) and E2 on differentiation and Nup133 signaling using mouse-derived primary oligodendrocyte
progenitor cells (OPCs). We show that the steroids could reverse the effect of hyperoxia-mediated
downregulation of Nup133 in cultured male OPCs. The addition of FZS and E2 protected cells from
oxidative stress. However, E2, in presence of 16α-OH-DHEA, showed a negative effect on male
cells. These results assert the importance of sex-based differences and their potential implications in
preterm stress response.
KW  - preterm birth
KW  - oligodendrocyte precursor cells
KW  - fetal zone steroids;
KW  - estradiol;
KW  - hyperoxia
KW  - sex-based difference
KW  - differentiation
UN  - https://nbn-resolving.org/urn:nbn:de:gbv:9-opus-62394
SN  - ISSN: 1422-0067
SS  - ISSN: 1422-0067
U6  - https://doi.org/https://doi.org/10.3390/ijms22126586
DO  - https://doi.org/https://doi.org/10.3390/ijms22126586
VL  - 22
IS  - 12
SP  - 17
S1  - 17
ER  -