Narattaphol CharoenphandhuSuparerk LaohapitakwornKamonshanok KraidithLa iad NakkrasaePrapaporn JongwattanapisanPhuntila TharabenjasinNateetip KrishnamraMahidol UniversityKhon Kaen University2018-05-032018-05-032011-06-17Biochemical and Biophysical Research Communications. Vol.409, No.4 (2011), 775-779109021040006291X2-s2.0-79959242266https://repository.li.mahidol.ac.th/handle/20.500.14594/11531Parathyroid hormone (PTH) was recently demonstrated to enhance the HCO3- secretion through the apical anion channel, cystic fibrosis transmembrane conductance regulator (CFTR), but how the HCO3- entered the epithelial cells was not well understood, in part, due to the lack of specific inhibitors of the basolateral HCO3- transporters. Moreover, the function of the PTH-stimulated HCO3- secretion has never been investigated in vivo. Here, we designed three specific pairs of small interfering RNA sequences to simultaneously knockdown three variants of the electrogenic Na + /HCO3- co-transporter (NBCe)-1 in the intestinal epithelium-like Caco-2 monolayer. The results showed that NBCe1 mRNA levels were markedly reduced, and the PTH-induced transepithelial current and voltage changes were diminished after triple knockdown as determined by quantitative real-time PCR and Ussing chamber technique, respectively. An in vivo ligated intestinal loop study further showed that there was an increased fluid secretion, presumably driven by HCO3- transport, in the ileum, but not in jejunum or colon, of rats administered intravenously with 2μg/kg body weight of rat PTH 1-34. Therefore, the present results suggested that PTH stimulated intestinal HCO3- secretion, particularly in the ileum, by inducing the basolateral HCO3- uptake via NBCe1. © 2011 Elsevier Inc.Mahidol UniversityBiochemistry, Genetics and Molecular BiologyArticleSCOPUS10.1016/j.bbrc.2011.05.087