ArticleTurkish journal of obstetrics and gynecology2023
Increase in transforming growth factor-β didnot affect trombospondin1 in preeclampsia placentas.
Article in Turkish journal of obstetrics and gynecology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 6 citations in OpenAlex.
- Interleukin-6 Downregulates T Helper 17 Cytokines via Indoleamine 2,3-Dioxygenase 1 at the Maternal-Fetal Interface.American journal of reproductive immunology (New York, N.Y. : 1989) · 2026Article
- Investigation of the Impact of miRNA-7151 and a Mutation in Its Target Gene lncRNABiomedicines · 2025Article
- Insights into Reproductive Immunology and Placental Pathology.International journal of molecular sciences · 2024Article
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5 authors at 1 institution in 1 country.
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Abstract
Objective: The abnormalities of the placental growth process are a theory causing pre-eclampsia. Antiangiogenic factors contributed to it, such as thrombospondin-1 (TSp-1) that could stimulate transforming growth factor-beta (TGF-β), or vice versa. Some research showed that an increase in TGF-β did not always figurized its signaling. Therefore, we conducted a study to examine the TGF-β signaling proteins through its receptors and TSp-1 expression in preeclampsia placentas. Materials and Methods: This observational study used 33 normal and 33 pre-eclampsia placental storaged samples, for examination of TGF-β and TGF-βR 1 and 2, SMAD2 using ELISA, and SMAD2 and TSp-1 mRNA using the reverse transcription polymerase chain reaction method. Data were analyzed using SPSS version 20.0, normality test by Kolmogorov-Smirnov, and significancy was analyzed using nonparametric Mann-Whitney test, or t-test for parametric, with confidence interval 95%. Spearman correlation was used for non-parametric data, besides the Pearson correlation for parametric data. Results: Results showed that there were significant differences between preeclampsia and normal placenta in TGF-β, its receptors, SMAD2, and TSp-1 mRNA. Normal-TGF-β=1.19 (0.713-2.051) pg/mg; preeclampsia-TGFB=2.69 (0.906-10.252) pg/mg; p=0.001; normal-TGFBR1=1.025 (0.622-1.402) ng/mg; preeclampsia-TGFBR1=1.223 (0.372-2.553) ng/mg; p=0.004; Normal-TGF-βR2=0.959 (0.644-1.634) pg/mg; preeclampsia-TGFBR2=1.490 (0.775-3.645) pg/mg; p=0.0001; normal-SMAD2=2.087 (1.279-4.300) ng/mg; preeclampsia-SMAD2=3.508 (1.842-22.489) ng/mg; p=0.0001. The SMAD2 mRNA relative expression (Livax) in the normal placenta was=0.71 (0.03-7.25); pre-eclampsia placenta (PE)=0.49 (0.01-40.71); p=0.075, the normal TSp-1 mRNA expression=1.08 (0.09-5.31); PE=0.21 (0.002-24.06); p=0.002. The correlation test showed a strong correlation between TGF-β with TGFBR1 and 2 in the normal placenta, conversely, there was no correlation in the preeclampsia placenta. There was also no correlation between SMAD2 and TSp-1 mRNA in both normal and pre-eclampsia. Conclusion: TGF-β signaling in the preeclampsia placenta was changed due to the increased of the protein signaling it self without correlation between TGF-β to its receptors and TSp-1 relative expression.
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