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HOME General Physiology and Biophysics 2014 General Physiology and Biophysics Vol.33, No.2, p.169–176, 2014
HOME General Physiology and Biophysics 2014 General Physiology and Biophysics Vol.33, No.2, p.169–176, 2014
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General Physiology and Biophysics Vol.33, No.2, p.169–176, 2014 |
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| Title: Placental infiltration of inflammatory markers in gestational diabetic women | ||
| Author: Ines Mrizak, Oussama Grissa, Benoit Henault, Mariem Fekih, Ali Bouslema, Imen Boumaiza, Monia Zaouali, Zouhair Tabka, Naim A. Khan | ||
| Abstract: Gestational diabetes mellitus (GDM) is pathology of glucose intolerance during pregnancy. It is influenced by maternal hyperglycemia and insulinemia through placental circulation. The study was undertaken to investigate the implication of pro-inflammatory factors in the placenta of GDM women. Thirty GDM women have delivered macrosomic babies, and 30 healthy age-matched pregnant women have delivered non macrosomic babies, were recruited in the study. The mRNAs encoding for IL-6, TLR4, TGF-β, CD68, CD14, EMR-1, CCL2, TCR-α, T-bet, GATA-3, leptin and adiponectin were quantified in placental samples by using RT-qPCR. The mRNA expression of the pro-inflammatory factors, i.e., IL-6, TLR4 and TGF-β, was increased in GDM placenta. The mRNA expression of markers of infiltration of macrophage, i.e., CD68, CD14 and EMR-1, was higher in the GDM placenta than the control placenta. The expression of mRNA of TCR-α, an indicator of T-cell infiltration, was significantly higher in the GDM placenta. Interestingly, the expression of mRNA of GATA-3, an indicator of Th2 phenotype differentiation, was unregulated in the GDM placenta. Leptin and adiponectin mRNAs were also significantly increased in the placenta of the GDM group. Our results revealed that there is an increase of inflammation in the GDM placenta which might be involved, in part, in the pathogenesis of macrosomia. |
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| Keywords: Gestational diabetes mellitus — Macrosomia — Inflammation — Placenta | ||
| Year: 2014, Volume: 33, Issue: 2 | Page From: 169, Page To: 176 | |
| doi:10.4149/gpb_2013075 |
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