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Biology of Reproduction 64, 179-187 (2001)
© 2001 Society for the Study of Reproduction, Inc.


Regular Article

Expression and Localization of Luteinizing Hormone Receptor in the Female Mouse Reproductive Tract1

Meilin Zhenga, Hong Shia, Deborah L. Segaloffa, and Bradley J. Van Voorhis2,,b

a Department of Physiology and Biophysics and b Department of Obstetrics and Gynecology, The University of Iowa, Iowa City, Iowa 52240

ABSTRACT

The presence of the LH receptor (LHR) in nongonadal tissues of the reproductive tract has been reported, but localization studies have not been performed. Our objectives were to demonstrate the presence of LHR in the reproductive tract and to localize receptor expression. Reproductive age rats and mice were obtained and 125I-hCG binding assays were performed on membrane preparations from the uterus, ovary, liver, and testis. In situ hybridizations were performed using 35S-labeled antisense and sense RNA probes prepared from nucleotides 1–591 of the mouse LHR cDNA. Specific hCG binding was detected in membrane preparations from the ovary, uterus, and testis but not in the liver in both the rat and mouse. In the ovary, LHR mRNA was localized in theca cells, large follicles, and corpora lutea as expected. In the uterus, LHR mRNA was expressed in stromal cells of the endometrium and in the uterine serosa. Uterine smooth muscle cells had low levels of expression, and the endometrial epithelium was negative. In the oviduct, high levels of LHR expression were noted on the serosa and in subepithelial cells. Oviductal smooth muscle had low expression, and the epithelium was negative. We conclude that functional, nongonadal LHR are expressed in the mouse reproductive tract. The presence and localization of LHR expression in the mouse reproductive tract lay the foundation for transgenic models to address the physiologic role of these receptors.

FOOTNOTES

First decision: 25 May 2000.

1 These studies were supported by National Institutes of Health grants HD33931 and HD22916 (D.L.S.) and a Carver Collaborative Project grant from the University of Iowa. The services and facilities of the University of Iowa Diabetes and Endocrinology Research Center, supported by DK-25295, are also acknowledged.

2 Correspondence: Bradley J. Van Voorhis, Department of Obstetrics and Gynecology, The University of Iowa, 200 Hawkins Drive, Iowa City, IA 52242. FAX: 319 353 6659; brad-van-voorhis{at}uiowa.edu




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