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Wiley InterScience | |||||||||||||||||||||||
![]() Annals of the New York Academy of SciencesPublished Online: 9 Jan 2006 © 2010 The New York Academy of Sciences
Abstract | References | Full Text: HTML, PDF (Size: 449K) | Related Articles | Citation Tracking Human Decidual Relaxin and Preterm Birth Copyright 2005 New York Academy of Sciences KEYWORDS decidua • fetal membranes • placenta • relaxin • INSL4 • EPIL • growth • infection • inflammation Abstract:
Abstract: Relaxin in human pregnancy is both a systemic hormone from the corpus luteum and an autocrine/paracrine hormone at the maternal-fetal interface formed by the decidua/placenta and fetal membranes. We have focused our studies on the autocrine/paracrine roles of relaxin, especially in the preterm premature rupture of the fetal membranes, which causes 30-40% of preterm births. By using different techniques and different tissue collections, our laboratory has shown that expression of the relaxin genes and proteins in the decidua and placenta is increased in patients with preterm premature rupture of the fetal membranes. Relaxin binding and the expression of LGR7 are primarily in the chorion and decidua and are downregulated after spontaneous labor and delivery both at term and preterm. However, expression of LGR7 in the fetal membranes is significantly greater in all clinical situations at preterm than term, suggesting an important role for relaxin in these tissues at that time. The roles of the relaxin system in three potential causes of preterm birth are discussed: in the growth and proliferation of the membranes important for fetal membrane accommodation to fetal and placental growth, in acute infection, and in the inflammatory response leading to the initiation of labor. |
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Immunology and Pathogenesis of |
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