HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 294/5/C1158    most recent 00020.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (5) Citing Articles via Google Scholar Google Scholar Articles by Thongon, N. Articles by Charoenphandhu, N. Search for Related Content PubMed PubMed Citation Articles by Thongon, N. Articles by Charoenphandhu, N.

MEMBRANE TRANSPORTERS, ION CHANNELS, AND PUMPS

Prolactin stimulates transepithelial calcium transport and modulates paracellular permselectivity in Caco-2 monolayer: mediation by PKC and ROCK pathways

¹Department of Physiology and ²Consortium for Calcium and Bone Research, Faculty of Science, Mahidol University, Bangkok, Thailand

Submitted 15 January 2008 ; accepted in final form 18 March 2008

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.

charge selectivity; dilution potential; paracellular transport; phosphoinositide 3-kinase; protein kinase C; long form of prolactin receptor; RhoA; short interference RNA; transcellular transport

This article has been cited by other articles:

				N. Charoenphandhu, L.-i. Nakkrasae, K. Kraidith, J. Teerapornpuntakit, K. Thongchote, N. Thongon, and N. Krishnamra Two-step stimulation of intestinal Ca2+ absorption during lactation by long-term prolactin exposure and suckling-induced prolactin surge Am J Physiol Endocrinol Metab, September 1, 2009; 297(3): E609 - E619. [Abstract] [Full Text] [PDF]

				N. Thongon, L.-i. Nakkrasae, J. Thongbunchoo, N. Krishnamra, and N. Charoenphandhu Enhancement of calcium transport in Caco-2 monolayer through PKC{zeta}-dependent Cav1.3-mediated transcellular and rectifying paracellular pathways by prolactin Am J Physiol Cell Physiol, June 1, 2009; 296(6): C1373 - C1382. [Abstract] [Full Text] [PDF]