Thongon Narongrit, Ketkeaw Pattamaporn, Nuekchob Chanin
Division of Physiology, Department of Biomedical Sciences, Faculty of Allied Health Sciences, Burapha University, 169 Long-Hard Bangsaen Rd., Saensook, Muang, Chonburi, 20131, Thailand,
J Physiol Sci. 2014 Mar;64(2):129-39. doi: 10.1007/s12576-013-0301-8. Epub 2013 Dec 28.
Intestinal passive Mg(2+) absorption, which is vital for normal Mg(2+) homeostasis, has been shown to be regulated by luminal proton. We aimed to study the regulatory role of intestinal acid sensors in paracellular passive Mg(2+) transport. Omeprazole enhanced the expressions of acid-sensing ion channel 1a (ASIC1a), ovarian cancer G protein-coupled receptor 1 (OGR1), and transient receptor potential vanilloid 4 in Caco-2 cells. It also inhibited passive Mg(2+) transport across Caco-2 monolayers. The expression and activation of OGR1 resulted in the stimulation of passive Mg(2+) transport via phospholipase C- and protein kinase C-dependent pathways. ASIC1a activation, on the other hand, enhanced apical HCO3 (-) secretion that led, at least in part, by a Ca(2+)-dependent pathway to an inhibition of paracellular Mg(2+) absorption. Our results provided supporting evidence for the roles of OGR1 and ASIC1a in the regulation of intestinal passive Mg(2+) absorption.
肠道被动性镁离子吸收对正常的镁离子稳态至关重要，已表明其受肠腔质子调节。我们旨在研究肠道酸感受器在细胞旁被动性镁离子转运中的调节作用。奥美拉唑增强了Caco-2细胞中酸敏感离子通道1a（ASIC1a）、卵巢癌G蛋白偶联受体1（OGR1）和瞬时受体电位香草酸受体4的表达。它还抑制了镁离子跨Caco-2单层细胞的被动转运。OGR1的表达和激活通过磷脂酶C和蛋白激酶C依赖性途径刺激了被动性镁离子转运。另一方面，ASIC1a的激活增强了顶端碳酸氢根分泌，这至少部分地通过钙依赖性途径导致细胞旁镁离子吸收受到抑制。我们的结果为OGR1和ASIC1a在调节肠道被动性镁离子吸收中的作用提供了支持性证据。
