ArticleReproductive sciences (Thousand Oaks, Calif.)2022
Resistin Modulates Low-Density Lipoprotein Cholesterol Uptake in Human Placental Explants via PCSK9.
Article in Reproductive sciences (Thousand Oaks, Calif.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Alterations in infant adipokine concentrations in the first postnatal week with exposure to diabetes in pregnancy.Journal of perinatology : official journal of the California Perinatal Association · 2025Article
- Relationship Between Glucose/Lipid Metabolism and Placental Biomarkers in Gestational Diabetes and Preeclampsia.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Article
- Adipokine Levels of RBP4, Resistin and Nesfatin-1 in Women Diagnosed With Gestational Diabetes.Physiological research · 2024Article
- Association of Platelet-Monocyte Ratio with Dyslipidemia in Saudi Arabia: A Large, Population-Based Study.Life (Basel, Switzerland) · 2023Article
- Self-assembled human placental model from trophoblast stem cells in a dynamic organ-on-a-chip system.Cell proliferation · 2023Article
- Effect of Lifestyle Interventions during Pregnancy on Maternal Leptin, Resistin and Offspring Weight at Birth and One Year of Life.Biomedicines · 2023Article
- The Role of Adipokines in Inflammatory Mechanisms of Obesity.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Maternal metabolic status influences pregnancy and, consequently, the perinatal outcome. Resistin is a pro-inflammatory adipokine predominantly expressed and secreted by mononuclear cells, adipose tissue, and placental trophoblastic cells during pregnancy. Recently, we reported an inverse association between maternal resistin levels and fetal low-density lipoprotein cholesterol (LDL-C). Then, in this work, we used a human placental explant model and the trophoblast cell line JEG-3 to evaluate whether resistin affects placental LDL-C uptake. Resistin exposure induced the transcription factor SREBP-2, LDLR, and PCSK9 mRNA expression, and changes at the protein level were confirmed by immunohistochemistry and Western blot. However, for LDLR, the changes were not consistent between mRNA and protein levels. Using a labeled LDL-cholesterol (BODIPY FL LDL), uptake assay demonstrated that the LDL-C was significantly decreased in placental explants exposed to a high dose of resistin and a lesser extent in JEG-3 cells. In summary, resistin induces PCSK9 expression in placental explants and JEG-3 cells, which could be related to negative regulation of the LDLR by lysosomal degradation. These findings suggest that resistin may significantly regulate the LDL-C uptake and transport from the maternal circulation to the fetus, affecting its growth and lipid profile.
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