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The Human Fetal Membranes: A Target Tissue for Relaxin^*

Departments of Biochemistry-Biophysics Honolulu, Hawaii 96822
Anatomy-Reproductive Biology, University of Hawaii Honolulu, Hawaii 96822

Address all correspondence and requests for reprints to:Dr. Gillian D.Bryant-Greenwood, Department of Anatomy and Reproductive Biology, University of Hawaii School of Medicine, 1960 East-West Road, Honolulu, Hawaii 96822.

The purpose of this study was to adduce further evidence for a paracrine role for human decidual relaxin (Rlx) in the remodelling of collagen in the fetal membranes in the peripartal period. The binding of [¹²⁵I]porcine Rlx to membraneenriched fractions from fetal membranes as well as from dispersed cells from the fetal membranes was used to demonstrate the presenceof specific Rlx receptors. Rlx added in vitro to cultured amnion/chorion cells increased the release of plasminogen activator and collagenase into the medium. Rlx had no effect on the release of β-glucuronidase.

An in vivo correlate of these in vitro results was obtained, the detection of plasminogen activator and collagenase in amniotic fluids. The active fraction of collagenase was increased in amniotic fluids collected after spontaneous rupture of the membranes. PRL, hCG, estrogen, and progesterone added in equimolar amounts to cultured amnion/chorion cells from elective cesarean sections and normal term deliveries also effected the release of plasminogen activator and collagenase. The greatest effects were found in cells from cesarean section tissue, in terms of thestimulation of plasminogen activator release by Rlx and PRL and of collagenase release by prostaglandin F₂ and, to a lesser extent, by Rlx, PRL, and hCG.

We conclude that human fetal membranes are targets for a number of hormones, including the decidual paracrine hormones Rlx, PRL, and prostaglandin F₂ as well as estrogen, progesterone, and hCG. These hormones act to release or inhibit thenzymes involved in collagen breakdown before rupture of the fetal membranes.

^* This work was supported by NIH Grant HD-06633 and the East-West Center Honolulu, HI.

Received January 15, 1985.

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