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Department of Physiology, Faculty of Medicine, Srinakharinwirot University, Sukhumvit 23, Wattana, Bangkok 10110, Thailand¹ Department of Physiology, Faculty of Veterinary Science, Chulalongkorn University, Henri-Dunant Road, Bangkok 10330, Thailand² , Department of Physiology³ Consortium for Calcium and Bone Research, Faculty of Science, Mahidol University, Rama VI Road, Bangkok 10400, Thailand

(Correspondence should be addressed to C Deachapunya; Email: chatsri{at}swu.ac.th)

The effect of prolactin (PRL) on ion transport across the porcine glandular endometrial epithelial cells was studied in primary cell culture using the short-circuit current technique. Addition of 1 µg/ml PRL either to the apical solution or to the basolateral solution produced a peak followed by a sustained increase in Isc, but with a lesser response when PRL was added apically. Basolateral addition of PRL increased the Isc in a concentration-dependent manner with a maximum effect at 1 µg/ml and an effective concentration value of 120 ng/ml. The PRL-stimulated Isc was significantly reduced by pretreatment with an apical addition of 5-nitro-2-(3-phenylpropylamino) benzoic acid (200 µM), diphenylamine-2-carboxylic acid (1 mM) or 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (200 µM), Cl^– channel blockers, but not by amiloride (10 µM), a Na⁺ channel blocker. In addition, pretreatment with bumetanide (200 µM), a Na⁺–K⁺–2Cl^– cotransporter inhibitor, in the basolateral solution significantly reduced the PRL-stimulated Isc. Replacement of Cl^– or in the bathing solutions also decreased the Isc response to PRL. Pretreatment of the monolayer with AG490 (50 µM), an inhibitor of JAK2 activity significantly inhibited the PRL-induced increase in Isc. Western blot analysis of the porcine endometrial epithelial cells revealed the presence of short isoform of PRL receptor (PRLR-S) that could be regulated by 17β-estradiol. The results of this investigation showed that PRL acutely stimulated anion secretion across the porcine endometrial epithelial cells possibly through PRLR-S present in both apical and basolateral membranes. The PRL response appeared to be mediated by the JAK2-dependent pathway.