NHE-3 isoform of the NA+/H+ exchanger in human gallbladder

Silviani, V.; Gastaldi, Marguerite; Planells, Richard; Marteau, C.; Massacrier, Annick; Cohen, Patrick; Cau, Pierre; Gérolami, A

doi:10.1016/s0168-8278(97)80463-1

Cited by 15 publications

(6 citation statements)

References 21 publications

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“…Na + /H + exchange, and NHE3 in particular, has also been detected in the gallbladder epithelium in human (277), calf (17), and prairie dog (1). Primary epithelial cells from the prairie dog gallbladder showed H + gradient-dependent 22 Na uptake mediated by NHE1 (6%), NHE2 (66%), and NHE3 (~28% of total uptake), as determined by studies with DMA and HOE-694 inhibitors (211).…”

Section: Na+/h+ Exchange Physiology In the Gallbladdermentioning

confidence: 99%

SLC9 Gene Family: Function, Expression, and Regulation

Kiela

2018

Comprehensive Physiology

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The Slc9 family of Na /H exchangers (NHEs) plays a critical role in electroneutral exchange of Na and H in the mammalian intestine as well as other absorptive and secretory epithelia of digestive organs. These transport proteins contribute to the transepithelial Na and water absorption, intracellular pH and cellular volume regulation as well as the electrolyte, acid-base, and fluid volume homeostasis at the systemic level. They also influence the function of other membrane transport mechanisms, affect cellular proliferation and apoptosis as well as cell migration, adherence to the extracellular matrix, and tissue repair. Additionally, they modulate the extracellular milieu to facilitate other nutrient absorption and to regulate the intestinal microbial microenvironment. Na /H exchange is inhibited in selected gastrointestinal diseases, either by intrinsic factors (e.g., bile acids, inflammatory mediators) or infectious agents and associated bacterial toxins. Disrupted NHE activity may contribute not only to local and systemic electrolyte imbalance but also to the disease severity via multiple mechanisms. In this review, we describe the cation proton antiporter superfamily of Na /H exchangers with a particular emphasis on the eight SLC9A isoforms found in the digestive tract, followed by a more integrative description in their roles in each of the digestive organs. We discuss regulatory mechanisms that determine the function of Na /H exchangers as pertinent to the digestive tract, their regulation in pathological states of the digestive organs, and reciprocally, the contribution of dysregulated Na /H exchange to the disease pathogenesis and progression. © 2018 American Physiological Society. Compr Physiol 8:555-583, 2018.

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Section: Na+/h+ Exchange Physiology In the Gallbladdermentioning

confidence: 99%

SLC9 Gene Family: Function, Expression, and Regulation

Kiela

2018

Comprehensive Physiology

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“…Na + /H + , probably also by an allosteric modulation at the cytosolic site [22,23]. NHE3 [20,21,24,25] and NHE2 [21] seem to be the main apical isoforms of the Na + /H + exchanger, involved in transepithelial salt absorption. Concerning this function, a potential cooperation between these two isoforms has been postulated [26].…”

Section: Systems Promoting Ion Absorptions In the Gallbladdermentioning

confidence: 99%

“…Concerning this function, a potential cooperation between these two isoforms has been postulated [26]. NHE1, possibly responsible of intracellular pH homeostasis, has been detected in rabbit, human and calf gallbladder [20,24,25]. Extracellular HCO 3 -has a stimulatory effect on transepithelial NaCl transport with an apical primary action [27,28] but using a bicarbonate free luminal medium the Cl -influx through the apical membrane is strongly reduced but not completely abolished, at least in rabbit gallbladder [29,30].…”

Section: Systems Promoting Ion Absorptions In the Gallbladdermentioning

confidence: 99%

Ion Transport Across the Gallbladder Epithelium

Meyer¹,

Guizzardi²,

Rodighiero³

et al. 2005

curr drug targets immune endocr metabol disord

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The function of the gallbladder is not only to store bile, but also to concentrate it during the interdigestive phase by means of salt-dependent water reabsorption. On the contrary, secretions of water and salt take place during the digestive phase. Dysregulation of ion absorption or secretion are common in many gallbladder diseases, such as colelithiasis. Transepithelial absorptions are determined by the Na+/K+ pump on the basolateral membrane, and by several apical membrane Na(+)-coupled transporters. Among these, some isoforms of Na+/H+ and Cl-/HCO3(-) exchangers have been studied. The presence of a Na(+)-Cl(-) simport has been molecularly and functionally characterized in some animal species. The ion transepithelial secretion is mainly dependent on an apical chloride transport attributable to a CFTR-like cAMP-activated channel with high permeability to HCO3(-). The apical membrane electrical potential is one of the factors influencing anion secretion and is maintained by the activity of cAMP-dependent K+ channels. The regulation of the activity of these channels is complex, because of their sensitivity to voltage, and to intracellular calcium and pH. The coordinated interplay underlying the regulation of transporters and channels needs to be clarified yet, as well as the interactions between transporters, channels and aquaporins.

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“…Na + /H + exchanger isoform 3 (NHE3) is an Na + /H + exchanger isoform that is present in the apical membrane of small intestinal, colonic, and gallbladder Na + ‐absorbing cells. 1,2 In the small intestine and colon of human, dog, rabbit, rat, mouse, and chicken, NHE3 is present in the brush border (BB) of the villus (small intestinal) and surface (colon and gallbladder) epithelial cells and also in the BB of epithelial cells of the upper crypt. These are the epithelial cells that are involved in Na + absorption.…”

Section: Physiology Of Intestinal Nhe3mentioning

confidence: 99%

Short‐Term Regulation of NHE3 by EGF and Protein Kinase C but Not Protein Kinase A Involves Vesicle Trafficking in Epithelial Cells and Fibroblasts

Donowitz

Janecki

Akhter

et al. 2000

Annals of the New York Academy of Sciences

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NHE3 is an intestinal epithelial isoform Na+/H+ exchanger that is present in the brush border of small intestinal, colonic, and gallbladder Na+‐absorbing epithelial cells. NHE3 is acutely up‐ and downregulated in response to some G protein‐linked receptors, tyrosine kinase receptors, and protein kinases when studied in intact ileum, when stably expressed in PS120 fibroblasts, and in the few studies reported in the human colon cancer cell line Caco‐2. In most cases this is due to changes in Vmax of NHE3, although in response to cAMP and squalamine there are also changes in the K′ (H+)i of the exchanger. The mechanism of the Vmax regulation as shown by cell surface biotinylation and confocal microscopy in Caco‐2 cells and biotinylation in PS120 cells involves changes in the amount of NHE3 on the plasma membrane. In addition, in some cases there are also changes in turnover number of the exchanger. In some cases, the change in amount of NHE3 in the plasma membrane is associated with a change in the amount of plasma membrane. A combination of biochemical studies and transport/inhibitor studies in intact ileum and Caco‐2 cells demonstrated that the increase in brush border Na+/H+ exchange caused by acute exposure to EGF was mediated by PI 3‐kinase. PI 3‐kinase was also involved in FGF stimulation of NHE3 expressed in fibroblasts. Thus, NHE3 is another example of a transport protein that is acutely regulated in part by changing the amount of the transporter on the plasma membrane by a process that appears to involve vesicle trafficking and also to involve changes in turnover number.

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NHE-3 isoform of the NA+/H+ exchanger in human gallbladder

Cited by 15 publications

References 21 publications

SLC9 Gene Family: Function, Expression, and Regulation

SLC9 Gene Family: Function, Expression, and Regulation

Ion Transport Across the Gallbladder Epithelium

Short‐Term Regulation of NHE3 by EGF and Protein Kinase C but Not Protein Kinase A Involves Vesicle Trafficking in Epithelial Cells and Fibroblasts

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