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Reproduction


Title:Placental leukocyte infiltration accompanies gestational changes induced by hyperthyroidism
Author(s):Sanchez MB; Neira FJ; Moreno-Sosa T; Michel Lara MC; Viruel LB; Germano MJ; Pietrobon EO; Troncoso M; Soaje M; Jahn GA; Valdez SR; Mackern-Oberti JP;
Address:"Instituto de Medicina y Biologia Experimental de Cuyo CONICET, Universidad Nacional de Cuyo, Mendoza, Argentina. Facultad de Ciencias Veterinarias y Ambientales, Universidad Juan Agustin Maza, Mendoza, Argentina. Facultad de Farmacia y Bioquimica, Universidad Juan Agustin Maza, Mendoza, Argentina. Instituto de Histologia y Embriologia de Mendoza, Facultad de Ciencias Medicas, Universidad Nacional de Cuyo, Mendoza, Argentina. Facultad de Ciencias Exactas y Naturales, Universidad Nacional de Cuyo, Mendoza, Argentina. Instituto de Fisiologia, Facultad de Ciencias Medicas, Universidad Nacional de Cuyo, Mendoza, Argentina"
Journal Title:Reproduction
Year:2023
Volume:20230112
Issue:3
Page Number:235 - 248
DOI: 10.1530/REP-22-0210
ISSN/ISBN:1741-7899 (Electronic) 1470-1626 (Linking)
Abstract:"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 T4 0.25 mg/kg) Wistar rats were mated 8 days after starting T4 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"
Keywords:"Rats Animals Pregnancy Female *Placenta/metabolism Rats, Wistar Thyroid Hormones/metabolism *Hyperthyroidism/metabolism/pathology RNA, Messenger/metabolism Leukocytes/metabolism;"
Notes:"MedlineSanchez, Maria Belen Neira, Flavia Judith Moreno-Sosa, Tamara Michel Lara, Maria Cecilia Viruel, Luciana Belen Germano, Maria Jose Pietrobon, Elisa Olivia Troncoso, Mariana Soaje, Marta Jahn, Graciela Alma Valdez, Susana Ruth Mackern-Oberti, Juan Pablo eng Research Support, Non-U.S. Gov't England 2022/12/10 Reproduction. 2023 Jan 12; 165(3):235-248. doi: 10.1530/REP-22-0210. Print 2023 Mar 1"

 
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