Linked Life Data

21389278

Source:http://linkedlifedata.com/resource/pubmed/id/21389278

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2011-6-28
pubmed:abstractText
Besides being a Ca²-regulating hormone, parathyroid hormone (PTH) has also been shown to regulate epithelial transport of certain ions, such as Cl, HCO?, and Na, particularly in the kidney. Although the intestinal epithelium also expressed PTH receptors, little was known regarding its mechanism in the regulation of intestinal ion transport. We investigated the ion regulatory role of PTH in intestinal epithelium-like Caco-2 monolayer by Ussing chamber technique and alternating current impedance spectroscopy. It was found that Caco-2 cells rapidly responded to PTH within 1 min by increasing apical HCO?- secretion. CFTR served as the principal route for PTH-stimulated apical HCOV efflux, which was abolished by various CFTR inhibitors, namely, NPPB, glycine hydrazide-101 (GlyH-101), and CFTRinh-172, as well as by small interfering RNA against CFTR. Concurrently, the plasma membrane resistance was decreased with no changes in the plasma membrane capacitance or paracellular permeability. HCOV was probably supplied by basolateral uptake via the electrogenic Na?-HCO?? cotransporter and by methazolamide-sensitive carbonic anhydrase, while the resulting intracellular H? might be extruded by both apical and basolateral Na/H exchangers. Furthermore, the PTH-stimulated HCO?-secretion was markedly reduced by protein kinase A (PKA) inhibitor (PKI 14-22 amide) and phosphoinositide 3-kinase (PI3K) inhibitors (wortmannin and LY-294002), but not by intracellular Ca²? chelator (BAPTA-AM) or protein kinase C inhibitor (GF-109203X). In conclusion, the present study provided evidence that PTH directly and rapidly stimulated apical HCO?- secretion through CFTR in PKA- and PI3K-dependent manner, which was a novel noncalciotropic, ion regulatory action of PTH in the intestinal epithelium.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/3-((3-trifluoromethyl)phenyl)-5-((3-..., http://linkedlifedata.com/resource/pubmed/chemical/5-nitro-2-(3-phenylpropylamino)benzo..., http://linkedlifedata.com/resource/pubmed/chemical/Benzoic Acids, http://linkedlifedata.com/resource/pubmed/chemical/Bicarbonates, http://linkedlifedata.com/resource/pubmed/chemical/Cystic Fibrosis Transmembrane..., http://linkedlifedata.com/resource/pubmed/chemical/Glycine, http://linkedlifedata.com/resource/pubmed/chemical/Nitrobenzoates, http://linkedlifedata.com/resource/pubmed/chemical/Parathyroid Hormone, http://linkedlifedata.com/resource/pubmed/chemical/RNA, Small Interfering, http://linkedlifedata.com/resource/pubmed/chemical/Thiazolidines, http://linkedlifedata.com/resource/pubmed/chemical/glycine hydrazide
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1522-1563
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
301
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
C137-49
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
Parathyroid hormone (PTH) rapidly enhances CFTR-mediated HCO?? secretion in intestinal epithelium-like Caco-2 monolayer: a novel ion regulatory action of PTH.
pubmed:affiliation
Consortium for Calcium and Bone Research, Faculty of Science, Mahidol University, Bangkok, Thailand.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't