Publication: Prolactin stimulates transepithelial calcium transport and modulates paracellular permselectivity in Caco-2 monolayer: Mediation by PKC and ROCK pathways
3
Issued Date
2008-05-01
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ISSN
15221563
03636143
03636143
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2-s2.0-48249157392
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Mahidol University
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SCOPUS
Bibliographic Citation
American Journal of Physiology - Cell Physiology. Vol.294, No.5 (2008)
Suggested Citation
Narongrit Thongon, La Iad Nakkrasae, Jirawan Thongbunchoo, Nateetip Krishnamra, Narattaphol Charoenphandhu Prolactin stimulates transepithelial calcium transport and modulates paracellular permselectivity in Caco-2 monolayer: Mediation by PKC and ROCK pathways. American Journal of Physiology - Cell Physiology. Vol.294, No.5 (2008). doi:10.1152/ajpcell.00020.2008 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/18923
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Title
Prolactin stimulates transepithelial calcium transport and modulates paracellular permselectivity in Caco-2 monolayer: Mediation by PKC and ROCK pathways
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Abstract
Prolactin (PRL) was previously demonstrated to rapidly enhance calcium absorption in rat duodenum and the intestine-like Caco-2 monolayer. However, its mechanism was not completely understood. Here, we investigated nongenomic effects of PRL on the transepithelial calcium transport and paracellular permselectivity in the Caco-2 monolayer by Ussing chamber technique. PRL increased the transcellular and paracellular calcium fluxes and paracellular calcium permeability within 60 min after exposure but decreased the transepithelial resistance of the monolayer. The effects of PRL could not be inhibited by RNA polymerase II inhibitor (5,6-dichloro-1-β-D- ribobenzimidazole), confirming that PRL actions were nongenomic. Exposure to protein kinase C (PKC) or RhoA-associated coiled-coil forming kinase (ROCK) inhibitors (GF-109203X and Y-27632, respectively) abolished the stimulatory effect of PRL on transcellular calcium transport, whereas ROCK inhibitor, but not PKC inhibitor, diminished the PRL effect on paracellular calcium transport. Knockdown of the long isoform of PRL receptor (PRLR-L) also prevented the enhancement of calcium transport by PRL. In addition, PRL markedly increased paracellular sodium permeability and the permeability ratio of sodium to chloride, which are indicators of the paracellular charge-selective property and are known to be associated with the enhanced paracellular calcium transport. The permeability of other cations in the alkali metal series was also increased by PRL, and such increases were abolished by ROCK inhibitor. It could be concluded that PRL stimulated transepithelial calcium transport through PRLR-L and increased paracellular permeability to cations in the Caco-2 monolayer. These nongenomic actions of PRL were mediated by the PKC and ROCK signaling pathways. Copyright © 2008 the American Physiological Society.