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Expression of Heparin/Heparan Sulfate Interacting Protein/Ribosomal Protein L29 During the Estrous Cycle and Early Pregnancy in the Mouse¹

^a Department of Biological Sciences, University of Delaware, Newark, Delaware 19707 ^b Department of Obstetrics/Gynecology & Physiology, University of Kansas Medical Center, Kansas City, Kansas 66160-7338

ABSTRACT

Using a variety of approaches, we have examined the expression of the heparin/heparan sulfate (Hp/HS) interacting protein/ribosomal protein L29 (HIP/RPL29) in mouse uteri during the estrous cycle and early pregnancy. HIP/RPL29 selectively binds heparin and HS and may promote HS-dependent embryo adhesion. HIP/RPL29 was prominently expressed in both luminal and glandular epithelia under almost all conditions, including the phase of embryo attachment. In contrast, differences were noted in HIP/RPL29 expression in the stromal compartment both during the estrous cycle and during early pregnancy. Most notably, HIP/RPL29 accumulated in decidua, where it displayed a pattern complementary to that of pericellular deposition of the HS proteoglycan, perlecan. HIP/RPL29 protein was detected in implanted embryos at both initial and later stages of implantation; however, embryonic HIP/RPL29 mRNA accumulation was more pronounced at later stages (Day 7.5 postcoitum). In situ hybridization revealed similar spatial changes for HIP/RPL29 mRNA during these different physiological states. Whereas differences in the spatial pattern of HIP/RPL29 protein and mRNA expression were demonstrable, little change was detected in the level of HIP/RPL29 mRNA or protein in total endometrial extracts. Mouse blastocysts attached, but did not outgrow, on surfaces coated with recombinant murine HIP/RPL29. Surprisingly, soluble glycosaminoglycans including heparin, low molecular weight heparin, or chondroitin sulfate were not able to inhibit embryo attachment to HIP/RPL29-coated surfaces. These latter observations indicate that embryonic cell surface components other than HS proteoglycans can promote binding to HIP/RPL29 expressed by uterine cells.

FOOTNOTES

First decision: 8 August 2000.

¹ Supported by National Institutes of Health grants HD 25235 and HD 29963 to D.D.C., HD 29968 to S.K. Dey, and ES 07814 to S.K. Das. This work was performed in part as a component of the National Cooperative Program for Markers of Uterine Receptivity.

² Correspondence: Daniel Carson, Department of Biological Sciences, 117 Wolf Hall, University of Delaware, Newark, DE 19707. FAX: 302 831 2281; dcarson{at}udel.edu

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