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Expression of Functional Luteinizing Hormone (LH) Receptor and Its Messenger Ribonucleic Acid in Bovine Uterine Veins: LH Induction of Cyclooxygenase and Augmentation of Prostaglandin Production in Bovine Uterine Veins¹

Departments of Hormone Research (M.S., M.G., D.M., L.D., L.S.S.) and Molecular Virology (Y.M.), Kimron Veterinary Institute, Bet Dagan, Israel; and the Animal Science Department (M.J.F.), University of Florida, Gainesville, Florida 32611

Address all correspondence and requests for reprints to: Mordechai Shemesh, Department of Hormone Research, Kimron, Veterinary Institute, Bet Dagan 12, Israel. E-mail: shemesh{at}huji.agri.ac.il

We have previously reported that bovine endometrium contains LH/human CG binding receptors and LH induces cyclooxygenase and prostaglandin production in the bovine endometrium. The present study investigated 1) whether bovine uterine vein and artery contain LH receptor messenger RNA (mRNA) and receptor protein and 2) whether LH can regulate the formation of vasoactive eicosanoids by the uterine vein. The uterine vein endothelium, but not the uterine artery, contained LH receptor mRNA transcript essentially identical to that found in the bovine corpus luteum. The uterine vein endothelium also contained a 95-kDa immunoreactive receptor protein that bound to rat anti-LH receptor antibody in Western blots. The LH receptor mRNA and LH receptor were maximally expressed in the uterine vein from cows in proestrus/estrus compared with cows in luteal or postovulatory phases. Incubation of endothelial minces of uterine vein with LH resulted in a 2-fold increase in cyclooxygenase concentration as determined by Western blot using an antibody to ram seminal vesicle cyclooxygenase. The increase in cyclooxygenase was maximal in cows in proestrus/estrus compared with postovulatory and luteal phase cows. Incubation of proestrous/estrous uterine vein or artery minces with LH or mellitin (a phospholipase A₂ stimulator) caused increased production of eicosanoids. In the uterine vein, LH caused a significant increase in both PGF₂ (basal 4.1 ± 0.4 vs. 5.7 ± 0.4 ng/100 mg·6 h, P < 0.01; N = 9 cows) and PGE₂ (basal 5.7 ± 0.3 vs. 7.7 ± 0.8 ng/100 mg·6 h, P < 0.01; N = 6 cows) but had no effect on prostaglandin production by the artery. Mellitin increased PGF₂ production by both uterine vein and artery minces but had no effect on PGE₂ production in either tissue. Addition of steroids (progesterone, estradiol) or cytokines (tumor necrosis factor-, IL-6) to the uterine vascular tissues had essentially no effect on prostanoid production. In summary, bovine uterine vein from proestrous/estrous cows expressed the LH receptor and its mRNA. Expression of the receptor may have physiological significance as LH induces cyclooxygenase and increases prostaglandin release in the uterine vein. The maximal stimulation of the receptor and its mRNA at proestrus/estrus may serve to increase the amounts of prostanoids reaching the regressing corpus luteum either directly by increasing prostanoid production or indirectly by increasing the blood flow to the ovary.

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