Placental leukocyte infiltration accompanies gestational changes induced by hyperthyroidism

内科学 内分泌学 胎盘 生物 激素 蜕膜 胎儿 甲状腺 甲状腺激素受体 怀孕 医学 遗传学
作者
María Belén Sánchez,Flavia Judith Neira,Tamara Moreno-Sosa,María Cecilia Michel Lara,Luciana Belén Viruel,María José Germanó,Elisa Olivia Pietrobon,Mariana Troncoso,Marta Soaje,Graciela A. Jahn,Susana R. Valdéz,Juan Pablo Mackern‐Oberti
出处
期刊:Reproduction [Bioscientifica]
卷期号:165 (3): 235-248 被引量:2
标识
DOI:10.1530/rep-22-0210
摘要

In brief The endocrine and immunological disruption induced by hyperthyroidism could alter gestation, placenta, and fetal development. This study suggests an immunological role of thyroid hormones in gestation. Abstract Thyroid dysfunctions lead to metabolic, angiogenic, and developmental alterations at the maternal–fetal interface that cause reproductive complications. Thyroid hormones (THs) act through their nuclear receptors that interact with other steroid hormone receptors. Currently, immunological regulation by thyroid status has been characterized to a far less extent. It is well known that THs exert regulatory function on immune cells and modulate cytokine expression, but how hyperthyroidism (hyper) modulates placental immunological aspects leading to placental alterations is unknown. This work aims to throw light on how hyper modulates immunological and morphological placental aspects. Control and hyper (induced by a daily s.c. injection of T 4 0.25 mg/kg) Wistar rats were mated 8 days after starting T 4 treatment and euthanized on days 19 (G19) and 20 (G20) of pregnancy. We removed the placenta to perform qPCR, flow cytometry, immunohistochemistry, Western blot and histological analysis, and amniotic fluid and serum to evaluate hormone levels. We observed that hyper increases the fetal number, fetal weight, and placental weight on G19. Moreover, hyper induced an endocrine imbalance with higher serum corticosterone and changed placental morphology, specifically the basal zone and decidua. These changes were accompanied by an increased mRNA expression of glucocorticoid receptor and monocyte chemoattractant protein-1, an increased mRNA and protein expression of prolactin receptor, and an increase in CD45 + infiltration. Finally, by in vitro assays, we evidenced that TH induced immune cell activation. In summary, we demonstrated that hyper modulates immunological and morphological placental aspects and induces fetal phenotypic changes, which could be related to preterm labor observed in hyper.
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