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<p>This study aimed to determine the in vitro effects of visfatin on selected endocrine mediators in the human placenta. Using placental BeWo cells and villous explants from normal pregnancies and those complicated by intrauterine growth restriction (IUGR), preeclampsia (PE), and gestational diabetes mellitus (GDM), we determined the effects of visfatin on 3β-hydroxysteroid dehydrogenase (3β-HSD), aromatase (CYP19), human chorionic gonadotropin (hCG), human placental lactogen (hPL), placental growth hormone (GH2) expression, and the secretion of progesterone (P<sub>4</sub>), estradiol (E<sub>2</sub>) and mentioned protein hormones. We also investigated the effects of visfatin on the phosphorylation of protein kinase A (PKA), and hormone secretion after the pharmacological inhibition of insulin receptor (INSR), extracellular signal-regulated kinase 1/2 (ERK1/2), and PKA. We noted that visfatin increased or decreased the mRNA and protein expression of <i>HSD3B1</i>/3β-HSD, <i>CYP19A1</i>/CYP19, <i>CGB3</i>/hCG, <i>CSH1</i>/hPL, and <i>GH2</i>/GH2 in the tested groups. Additionally, visfatin lowered the secretion of P<sub>4</sub>, E<sub>2</sub>, hCG, hPL, and GH2 in BeWo cells and normal placenta, but modulated it in placenta explants from the pathological groups. The secretion of E<sub>2</sub>, hPL and GH2 was mediated by INSR, ERK1/2, and PKA, while P<sub>4</sub> by INSR and ERK1/2. These data indicated that visfatin acting via selected molecular pathways may be an important regulator of placental endocrine function during normal and complicated pregnancies.</p>

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VISFATIN: a novel modulator of placental endocrinology under physiological and pathological conditions—in vitro studies involving INSR, ERK1/2, and PKA signalling pathways

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月24日

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  • Monika Dawid,
  • Wiktoria Gieras,
  • Tomasz Milewicz,
  • Agnieszka Rak

摘要

This study aimed to determine the in vitro effects of visfatin on selected endocrine mediators in the human placenta. Using placental BeWo cells and villous explants from normal pregnancies and those complicated by intrauterine growth restriction (IUGR), preeclampsia (PE), and gestational diabetes mellitus (GDM), we determined the effects of visfatin on 3β-hydroxysteroid dehydrogenase (3β-HSD), aromatase (CYP19), human chorionic gonadotropin (hCG), human placental lactogen (hPL), placental growth hormone (GH2) expression, and the secretion of progesterone (P4), estradiol (E2) and mentioned protein hormones. We also investigated the effects of visfatin on the phosphorylation of protein kinase A (PKA), and hormone secretion after the pharmacological inhibition of insulin receptor (INSR), extracellular signal-regulated kinase 1/2 (ERK1/2), and PKA. We noted that visfatin increased or decreased the mRNA and protein expression of HSD3B1/3β-HSD, CYP19A1/CYP19, CGB3/hCG, CSH1/hPL, and GH2/GH2 in the tested groups. Additionally, visfatin lowered the secretion of P4, E2, hCG, hPL, and GH2 in BeWo cells and normal placenta, but modulated it in placenta explants from the pathological groups. The secretion of E2, hPL and GH2 was mediated by INSR, ERK1/2, and PKA, while P4 by INSR and ERK1/2. These data indicated that visfatin acting via selected molecular pathways may be an important regulator of placental endocrine function during normal and complicated pregnancies.