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G-protein subunit α-14 is dysregulated in human placentas from systemic lupus erythematosus pregnancies

Authors :
Ying-Jie Zhao
Tian Shan
Jia-Hui Xu
Colman Freel
Kai Wang
Huihui Li
Source :
Archives of Medical Science.
Publication Year :
2022
Publisher :
Termedia Sp. z.o.o., 2022.

Abstract

IntroductionSystemic lupus erythematosus (SLE) is associated with placental dysfunctions during pregnancy, which may cause multiple adverse fetal and maternal outcomes. G-protein subunits α-11 (GNA11) and -14 (GNA14) participate actively in angiogenesis via the modulation of endothelial function. This study aimed to determine whether GNA11 and GNA14 levels in placental tissues differed between SLE and normal term pregnancies.Material and methodsTwenty-four individuals, including 14 patients with SLE and 10 normal pregnant women, were included in this study. The expression levels of GNA11 and GNA14 in the placentas were examined using reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and Western blotting analyses. The localization of GNA11 and GNA14 in placental tissues was evaluated using immunohistochemistry. The correlations between relative mRNA and protein expression levels of GNA11,14 and the Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) scores were also analyzed.ResultsRT-qPCR revealed that the mRNA levels of GNA14, but not GNA11, were significantly decreased by 50% (P = 0.01) in SLE vs. normal term placentas. Western blotting showed that the protein levels of GNA14, but not GNA11, were significantly increased by 3.52-fold (P = 0.02) in SLE vs. normal term placentas. Using immunohistochemistry, positive staining for GNA11 and GNA14 was present in trophoblasts and villous stromal cells of the placental tissues. The expression levels of GNA11 and GNA14 were not significantly correlated with the SLEDAI scores (r2=0.02~0.24, P = 0.08~0.75).ConclusionsThe dysregulation of GNA14 in the placentas indicates a regulatory role during human SLE pregnancies.

Subjects

Subjects :
General Medicine

Details

ISSN :
18969151 and 17341922
Database :
OpenAIRE
Journal :
Archives of Medical Science
Accession number :
edsair.doi...........cb5809fb3c6e5749dc3dee8480351696
Full Text :
https://doi.org/10.5114/aoms/146404