PRIMATE DECIDUA AND FETAL MEMBRANES AS A PARACRINE SYSTEM

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. In the absence of infection, a localized low-level inflammatory response in the fetal membrane may be associated with premature rupture of membranes (PROM) in both term and preterm birth. This contrasts with the florid inflammatory response characteristic of infection-mediated preterm parturition. Decidual relaxin expression is increased in patients with PROM and preterm birth. The objective of this research is to ascertain whether intraamniotic administration of human recombinant relaxin in a pregnant nonhuman primate model causes changes in key pathways (developmental growth regulators, extracellular matrix modulators, and/or proinflammatory mediators) which may precede preterm premature rupture of the fetal membranes (PPROM).