Na+/H+ Exchange in Mammalian Digestive Tract

Kiela, Pawel R.

doi:10.1016/b978-0-12-382026-6.00066-x

Cited by 13 publications

(9 citation statements)

References 313 publications

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“…In HAT‐7 cells in the absence of

{HCO}_{3}^{-}

/CO 2 , we identified a basolateral Na + dependent, amiloride sensitive proton extruding entity suggesting the presence of Na + /H + exchanger activity at this membrane (Racz et al., ). This is consistent with the observation that the presence of a basolateral Na + /H + exchanger, usually NHE1, is an almost universal feature of the epithelial cells of the gastrointestinal tract (Kiela, Xu, & Ghishan, ). We also found that the application of the membrane permeable carbonic anhydrase inhibitor acetazolamide partially inhibited the basolateral base flux in HAT‐7 cells suggesting that this mechanism is present, and coupled to H + extrusion via a basolateral Na + ‐H + exchanger such as NHE1 (Bori et al., ).…”

Section: The Hat‐7 Cell Model To Functionally Study Ph Regulation By supporting

confidence: 91%

Importance of bicarbonate transport in pH control during amelogenesis — need for functional studies

et al. 2017

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Dental enamel, the hardest mammalian tissue, is produced by ameloblasts. Ameloblasts show many similarities to other transporting epithelia although their secretory product, the enamel matrix, is quite different. Ameloblasts direct the formation of hydroxyapatite crystals, which liberate large quantities of protons that then need to be buffered to allow mineralization to proceed. Buffering requires a tight pH regulation and secretion of bicarbonate by ameloblasts. Many investigations have used immunohistochemical and knockout studies to determine the effects of these genes on enamel formation, but up till recently very little functional data were available for mineral ion transport. To address this, we developed a novel 2D in vitro model using HAT-7 ameloblast cells. HAT-7 cells can be polarized and develop functional tight junctions. Furthermore, they are able to accumulate bicarbonate ions from the basolateral to the apical fluid spaces. We propose that in the future, the HAT-7 2D system along with similar cellular models will be useful to functionally model ion transport processes during amelogenesis. Additionally, we also suggest that similar approaches will allow a better understanding of the regulation of the cycling process in maturation-stage ameloblasts, and the pH sensory mechanisms, which are required to develop sound, healthy enamel. K E Y W O R D Sameloblast, amelogenesis, bicarbonate, enamel, functional model, HAT-7, in vitro, ion transport, microfluorometry, pH regulation, transepithelial resistance, transwell

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“…In HAT‐7 cells in the absence of

{HCO}_{3}^{-}

Section: The Hat‐7 Cell Model To Functionally Study Ph Regulation By supporting

confidence: 91%

Importance of bicarbonate transport in pH control during amelogenesis — need for functional studies

et al. 2017

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“…One μM HOE‐642 inhibits NHE1, whereas 50 μM HOE‐642 inhibits both NHE1 and 2 but not NHE3 26, 27. Although there are nine different NHE isoforms in mammalian digestive tract,28 only NHE1–3 are localized to the membrane of the cells 29. Therefore, the activities (A) of NHE isoforms can be calculated from the recoveries (R) as follows: …”

Section: Methodsmentioning

confidence: 99%

New therapeutic targets in ulcerative colitis: The importance of ion transporters in the human colon

Farkas¹,

Yeruva²,

Rakonczay³

et al. 2011

Inflammatory Bowel Diseases

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Background: The absorption of water and ions (especially Na+ and Cl−) is an important function of colonic epithelial cells in both physiological and pathophysiological conditions. Despite the comprehensive animal studies, there are only scarce available data on the ion transporter activities of the normal and inflamed human colon. Methods: In this study, 128 healthy controls and 69 patients suffering from ulcerative colitis (UC) were involved. We investigated the expressional and functional characteristics of the Na+/H+ exchangers (NHE) 1–3, the epithelial sodium channel (ENaC), and the SLC26A3 Cl−/HCO 3− exchanger downregulated in adenoma (DRA) in primary colonic crypts isolated from human biopsy and surgical samples using microfluorometry, patch clamp, and real‐time reverse‐transcription polymerase chain reaction (RT‐PCR) techniques. Results: Data collected from colonic crypts showed that the activities of electroneutral (via NHE3) and the electrogenic Na+ absorption (via ENaC) are in inverse ratio to each other in the proximal and distal colon. We found no significant differences in the activity of NHE2 in different segments of the colon. Surface cell Cl−/HCO 3− exchange is more active in the distal part of the colon. Importantly, both sodium and chloride absorptions are damaged in UC, whereas NHE1, which has been shown to promote immune response, is upregulated by 6‐fold. Conclusions: These results open up new therapeutic targets in UC. (Inflamm Bowel Dis 2011;)

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“… 35 Also, NHE2 KO mice neither show alterations in intestinal Na + absorption nor a diarrheal phenotype. 26 , 28 Therefore, dysregulation of NHE2 function and/or expression is not of great significance for altered electrolyte absorption observed in IBD. However, contribution of impaired NHE1 expression in IBD associated diarrhea warrants further experimental validation.…”

Section: Ibd and Altered Electrolyte Transport In The Intestinementioning

confidence: 99%

Pathophysiology of IBD associated diarrhea

et al. 2018

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Inflammatory bowel diseases broadly categorized into Crohn's disease (CD) and ulcerative colitis (UC), are chronic inflammatory disorders of the gastrointestinal tract with increasing prevalence worldwide. The etiology of the disease is complex and involves a combination of genetic, environmental, immunological and gut microbial factors. Recurring and bloody diarrhea is the most prevalent and debilitating symptom in IBD. The pathogenesis of IBD-associated diarrhea is multifactorial and is essentially an outcome of mucosal damage caused by persistent inflammation resulting in dysregulated intestinal ion transport, impaired epithelial barrier function and increased accessibility of the pathogens to the intestinal mucosa. Altered expression and/or function of epithelial ion transporters and channels is the principle cause of electrolyte retention and water accumulation in the intestinal lumen leading to diarrhea in IBD. Aberrant barrier function further contributes to diarrhea via leak-flux mechanism. Mucosal penetration of enteric pathogens promotes dysbiosis and exacerbates the underlying immune system further perpetuating IBD associated-tissue damage and diarrhea. Here, we review the mechanisms of impaired ion transport and loss of epithelial barrier function contributing to diarrhea associated with IBD.

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Na+/H+ Exchange in Mammalian Digestive Tract

Cited by 13 publications

References 313 publications

Importance of bicarbonate transport in pH control during amelogenesis — need for functional studies

Importance of bicarbonate transport in pH control during amelogenesis — need for functional studies

New therapeutic targets in ulcerative colitis: The importance of ion transporters in the human colon

Pathophysiology of IBD associated diarrhea

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