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Regulation of prolactin on electrolyte transport across porcine endometrial epithelial cells
Author(s) -
Deachapunya Chatsri,
Poonyachoti Sutthasinee,
Krishnamra Nateetip
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a543
Subject(s) - bumetanide , dids , prolactin , endocrinology , medicine , chemistry , channel blocker , amiloride , western blot , epithelial sodium channel , receptor , cotransporter , biology , sodium , biochemistry , hormone , calcium , organic chemistry , membrane , gene
The regulation of prolactin (PRL) on electrolyte transport was investigated in primary culture of porcine glandular endometrial epithelial cells using Ussing chamber technique. PRL produced a peak and sustained increase in short circuit current (Isc) in a concentration dependent manner with an EC 50 value of 120 ng/ml. The Isc increased by PRL was inhibited by pretreatment with an apical addition of 200 μM NPPB or 1 mM DPC, Cl − channel blockers, but not by 10 μM amiloride, a Na + channel blocker, or 200 μM DIDS chloride channel blocker. In addition, replacement of Cl − and HCO 3 − or pretreatment with 200 M bumetanide, a Na + ‐K + ‐2Cl − cotransporter inhibitor, in the basolateral solution mostly abolished the PRL‐stimulated Isc. Pretreatment with 10 μM indomethacin also abolished the PRL‐induced increase in Isc. Addition of 50 μM AG490, an inhibitor of JAK2 activity, to both apical and basolateral solutions completely inhibited the PRL‐increased Isc. Western blot analysis and immunocytochemistry revealed the expression of short isoform PRL receptors. These results demonstrated the PRL stimulation of anion secretion in endometrial epithelial cells. The PRL effect may be mediated by JAK‐STAT dependent pathway or through the release of cyclooxygenase metabolites. This work was supported by The Thailand Research Fund (RTA 478008).