Transplacental Transfer of Per- and Polyfluoroalkyl Substances (PFASs): Differences between Preterm and Full-Term Deliveries and Associations with Placental Transporter mRNA Expression

2020 ◽  
Vol 54 (8) ◽  
pp. 5062-5070 ◽  
Author(s):  
Jing Li ◽  
Dan Cai ◽  
Chu Chu ◽  
Qingqing Li ◽  
Yang Zhou ◽  
...  
Author(s):  
Mareike Appel ◽  
Martin Forsthuber ◽  
Romualdo Ramos ◽  
Raimund Widhalm ◽  
Sebastian Granitzer ◽  
...  

2021 ◽  
Vol 19 (2) ◽  
pp. 55-60
Author(s):  
M. A. KAGANOVA ◽  

The purpose — to assess the level of mRNA expression of TLR2, TLR4, TLR7 genes by the placenta and fetal membranes during full-term physiological pregnancy complicated by premature rupture of the membranes (tPROM). Material and methods. The placental and fetal membranes’ samples were collected during cesarean section to assess the level of mRNA expression of TLR2, TLR4, TLR7 genes in 35 women with full-term pregnancy in City Clinical Hospital No. 1 named after N.I. Pirogov (Samara). The main group consisted of 20 pregnant women with tPROM, 15 women were included in the control group (without tPROM or the onset of labor). The level of mRNA expression of the TLR2, TLR4, TLR7 genes was determined by the method of reverse transcription PCR in real time (RT-PCR) in the laboratory of molecular genetic methods of DNA-Technology LLC, using a Proba NK set of reagents. Results. The level of TLR2 expression in the fetal membranes in the main group was 1,87 times higher than in the control group, of TLR4 — 0,69 times lower and of TLR7 — 1,57 times higher. In the placenta, the expression of mRNA TLR2, TLR4, TLR7 genes did not differ. When compared by loci, a significant increase in TLR7 expression in the placenta was noted compared to the fetal membranes. Conclusion. The expression of mRNA TLR2 and TLR7 was increased with PROM in the fetal membranes, while the placenta remained intact and apparently did not participate in the pathogenesis of PROM, but has a higher level of placental TLR7 in both groups, which is apparently associated with more intense antigenic viral stimulation of placental tissues during pregnancy compared with the membranes.


2018 ◽  
Vol 9 (4) ◽  
pp. 395-400 ◽  
Author(s):  
Z.-Y. Le ◽  
S. Dong ◽  
R. Zhang ◽  
X.-P. Cai ◽  
A. Gao ◽  
...  

AbstractIt was reported that high blood cholesterol levels increased the susceptibility to mitochondrial dysfunction. This study hypothesized that the gestational hypercholesterolemia (HC) could induce the mitochondrial dysfunction in term human placenta. The eligible pregnant women were recruited from Xuanwu Hospital in Beijing during their first prenatal visit (before their 10th week of pregnancy). In total, 19 pregnant women whose serum total cholesterol levels were higher than 7.25 mm at third trimester (measured at 36–38 weeks) were selected as gestational HC. Other 19 pregnant women with normal cholesterol level matched with age, pre-gestational body mass index, and the neonatal gender were included as the control group. Full-term placenta samples were collected. The mitochondrial DNA (mtDNA) copy number, messenger RNA (mRNA) expression of cytochrome c oxidase subunit I, adenosine triphosphate monophosphatase 6 (ATP6ase), citrate synthase, peroxisome proliferator-activated receptor-γ (PPARγ) co-activator 1α, PPARγ co-activator 1β and estrogen-related receptor-α, and the activity of mitochondrial respiratory chain enzyme complex were measured. Pregnancy outcomes were obtained by extraction from medical records and the labor ward register. The results showed that only placental mtDNA copy number and mRNA expression of ATP6ase were significantly decreased in HC group. No significant differences were detected of other measurements between the two groups. These findings indicated that gestational HC might not induce the damage of placental function seriously.


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