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Partial Characterization of a Uteroglobin-Like Protein in the Human Uterus and Its Temporal Relationship to Prostaglandin Levels in This Organ^*

Section on Developmental Genetics, Human Genetics Branch, National Institute of Child Health and Human Development, National Institutes of Health Bethesda, Maryland 20892
The Department of Obstetrics and Gynecology, University of Mississippi Medical Center (B.D.C.) Jackson, Mississippi 39215
The Southern California Fertility Institute (R.I.T.) Los Angeles, California 90025

Address all correspondence and requests for reprints to: Dr. Anil B. Mukherjee, National Institutes of Health, Building 10, Room 8C429, Bethesda, Maryland 20892.

During the past decade several corticosteroiddependent, low mol wt proteins with phospholipase-A₂ (PLA₂) inhibitory activity have been described. This family of proteins is collectively known as lipocortins. Blastokinin or uteroglobin (utg), a progesterone-induced protein, first discovered in the pregnant rabbit uterus, is also a potent PLA₂ inhibitor, but genetically distinct from lipocortins. Although utg has been found in rabbits, its presence in humans has not been well established. Here, we present biochemical, immunological, and immunohistological evidence for the detection of a utg-like protein in the human uterus. Since inhibition of PLA₂ may modulate tissue eicosanoid levels and since rabbit utg has been reported to be a potent PLA₂ inhibitor, we also studied the temporal relationship between utg and tissue prostaglandin E₂ and F_2a levels in estrogen- and progesterone-dominated endometrial tissue. We found an inverse temporal relationship between utglike protein and eicosanoid levels in this organ. Since some eicosanoids (e.g. prostaglandins, leukotrienes, etc.) are known to be involved in smooth muscle contractility and inflammatory processes, our findings may help to understand the pathogenesis of some human disorders in which abnormal eicosanoid production occurs.

^* This work was supported in part by a grant from the Vicksburg Hospital Foundation.

Received December 17, 1987.

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