ArticleEuropean journal of histochemistry : EJH2019
Increased expression of STAT3 and SOCS3 in placenta from hyperglycemic rats.
Article in European journal of histochemistry : EJH, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 5 citations in OpenAlex.
- Placental lipid handling, growth and inflammatory pathways are modified by a maternal Mediterranean diet.Scientific reports · 2026Trial
- Effects of DPP4 Inhibition on Inflammation and Oxidative Stress in Experimental Gestational Diabetes Mellitus.International journal of molecular sciences · 2026Article
- Evidence for coopetition at the maternal-fetal interface shaping placental invasion.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Fetal growth restriction and placental defects in obese mice are associated with impaired decidualisation: the role of increased leptin signalling modulators SOCS3 and PTPN2.Cellular and molecular life sciences : CMLS · 2024Article
- Pulmonary maternal immune activation does not cross the placenta but leads to fetal metabolic adaptation.Nature communications · 2024Article
- Twenty years of histochemistry in the third millennium, browsing the scientific literature.European journal of histochemistry : EJH · 2020Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Signal transducer and activator of transcription 3 (STAT3) is a transcription factor that is activated by interleukin (IL)-6 and IL-10 that generate nearly opposing responses. The suppressor of cytokine signaling 3 (SOCS3) is the negative regulator of STAT3 and plays an important role in the negative regulation of the inflammatory process. Evidence has shown the importance of STAT3 and SOCS3 during implantation and normal pregnancy. However, little is known about the relationship of both factors under hyperglycemic condition. The aim of this study was to evaluate the placenta regions exhibiting immunopositivity for STAT3 and SOCS3 in hyperglycemic rats, as well as correlate these proteins with IL-10 and IL-6 levels. It was observed increased expression of STAT3 at the labyrinth (approximately 47% of increase compared to control) and junctional zone (approximately 32% of increase compared to control) from hyperglycemic placentas. Similar results were observed to SOCS3 (approximately 71% -labyrinth- and 53% -junctional zone- of increase compared to control). The levels of IL-10 were augmented at hyperglycemic placentas (approximately 1.5 fold of increase) and they were positively correlated with the increase of STAT3 at the labyrinth and SOCS at junctional zone. Therefore, under hyperglycemic conditions, the relation between STAT3 and SOCS3 was changed, leading to unbalance of the cytokine profile.
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Registered trials
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