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Vectorial Secretion of Prostaglandins by Polarized Rodent Uterine Epithelial Cells^*

Department of Biochemistry and Molecular Biology, University of Texas M.D. Anderson Cancer Center (A.L.J., G.L.D., D.D.C.) Houston, Texas 77030
The Department of Cell Biology, Baylor College of Medicine (S.R.G., J.J.) Houston, Texas 77030

Address all correspondence and requests for reprints to: Dr. Daniel D. Carson, Department of Biochemistry and Molecular Biology, Box 117, University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas 77030.

Abstract

Uterine epithelial cells (UEC) isolated from mature mice as well as immature mice and rats were cultured on EHS matrix-coated nitrocellulose filters in order to determine their ability to secrete prostaglandin (PG) F2 and PGE₂ in a polarized manner. Ultrastructural analyses were performed to validate the polar nature of mouse UEC and demonstrate the presence of separate apical and basolateral plasma membrane domains. These properties included the presence of tightly juxtaposed lateral membranes, apical microvilli, and a relatively flat basal surface. Biochemical indices of polarity included the preferential (-5:1) basal uptake of [³⁵S]methionine as well as a preferential (-9:1) apical secretion of protein. UEC isolated from mice during the estrous and diestrous stages of the estrous cycle did not differ in their degree of polarity, as measured by these morphological and biochemical indices. UEC of estrous and diestrous mice as well as immature mice and rats preferentially secreted PGF₂ to the basal medium to an approximately 4-fold greater extent than to the apical medium. PGE₂ was secreted at least 10-fold less than PGF₂, and a preferential basal secretion could not be demonstrated. Polarized UEC accumulated relatively large cellular pools of PGF₂, while nonpolarized cells grown on matrix-coated plastic did not. This difference was reflected by the inability of an inhibitor of PG biosynthesis, indomethacin, to inhibit PGF₂ secretion by polarized cells during short (4-h) incubations. In contrast, this drug effectively inhibited secretion in nonpolarized cells or polarized cells incubated with indomethacin for longer (24-h) intervals. Therefore, cellular PGF₂ pools apparently support continued secretion of this lipid even when de novo synthesis is transiently inhibited. Preferential basal secretion of PGF₂ was due to the polar nature of UEC, since disruption of tight junctions with EGTA modified the basal to apical ratio of PGF₂ secretion to near unity. Sodium azide inhibited the secretion of PGF₂, indicating that PGF₂ secretion was energy dependent. PGF₂ secretion was not coupled to protein synthesis or secretion, since cycloheximide did not inhibit this process in polarized or nonpolarized cells. These studies describe the first evidence for polarized secretion of lipidderived hormones by epithelial cells. The preferential basal secretion of PGF₂ may play an important role in regulating UEC interactions with the underlying stroma. (Endocrinology 126: 2125–2136, 1990)

Footnotes

^* Presented in part at the Annual Meeting of the American Society of Cell Biology, 1989, San Francisco, CA (Abstract 4467). This work was supported by NICHHD Postdoctoral Training Grant HD-07207 and NIH Training Grant HD-07324 (to A.L.J.); American Cancer Society Grant BC-503 (to D.D.C.); and NIH Grant HD-25189 (to S.R.G.).

Received October 10, 1989.

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