ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2008
Mice lacking the Na+/H+ exchanger 2 have impaired recovery of intestinal barrier function.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
- The function of chloride channels in digestive system disease (Review).International journal of molecular medicine · 2025Review
- The Role of Plasma Membrane Sodium/Hydrogen Exchangers in Gastrointestinal Functions: Proliferation and Differentiation, Fluid/Electrolyte Transport and Barrier Integrity.Frontiers in physiology · 2022Review
- Pathophysiological role of ion channels and transporters in gastrointestinal mucosal diseases.Cellular and molecular life sciences : CMLS · 2021Review
- Larazotide acetate induces recovery of ischemia-injured porcine jejunum via repair of tight junctions.PloS one · 2021Article
- The Integral Role of Tight Junction Proteins in the Repair of Injured Intestinal Epithelium.International journal of molecular sciences · 2020Review
- Moderate-to-severe asthma in individuals of European ancestry: a genome-wide association study.The Lancet. Respiratory medicine · 2019Article
- SLC9 Gene Family: Function, Expression, and Regulation.Comprehensive Physiology · 2018Review
- NaJournal of cellular physiology · 2017Article
- Trefoil Factor Peptides and Gastrointestinal Function.Annual review of physiology · 2017Review
- Large Animal Models: The Key to Translational Discovery in Digestive Disease Research.Cellular and molecular gastroenterology and hepatology · 2016Article
- Intestinal brush-border Na+/H+ exchanger-3 drives H+-coupled iron absorption in the mouse.American journal of physiology. Gastrointestinal and liver physiology · 2016Article
- Traditional and emerging roles for the SLC9 Na+/H+ exchangers.Pflugers Archiv : European journal of physiology · 2014Review
- Regulation of paracellular permeability: factors and mechanisms.Molecular biology reports · 2013Review
- Intestinal mast cells mediate gut injury and systemic inflammation in a rat model of deep hypothermic circulatory arrest.Critical care medicine · 2013Article
- Acute effects of rotavirus and malnutrition on intestinal barrier function in neonatal piglets.World journal of gastroenterology · 2013Article
- Claudins in intestines: Distribution and functional significance in health and diseases.Tissue barriers · 2013Review
- Extracellular acidosis stimulates NHE2 expression through activation of transcription factor Egr-1 in the intestinal epithelial cells.PloS one · 2013Article
- Keratinocyte growth factor improves epithelial structure and function in a mouse model of intestinal ischemia/reperfusion.PloS one · 2012Article
- Trefoil factor 2 requires Na/H exchanger 2 activity to enhance mouse gastric epithelial repair.The Journal of biological chemistry · 2011Article
- Somatostatin stimulates intestinal NHE8 expression via p38 MAPK pathway.American journal of physiology. Cell physiology · 2011Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Ischemic injury induces breakdown of the intestinal barrier. Recent studies in porcine postischemic tissues indicate that inhibition of NHE2 results in enhanced recovery of barrier function in vitro via a process involving interepithelial tight junctions. To further study this process, recovery of barrier function was assessed in wild-type (NHE2(+/+)) and NHE2(-/-) mice in vivo and wild-type mice in vitro. Mice were subjected to complete mesenteric ischemia in vivo, after which barrier function was measured by blood-to-lumen mannitol clearance over a 3-h recovery period or measurement of transepithelial electrical resistance (TER) in Ussing chambers immediately following ischemia. Tissues were assessed for expression of select junctional proteins. Compared with NHE2(+/+) mice, NHE2(-/-) mice had greater intestinal permeability during the postischemic recovery process. In contrast to prior porcine studies, pharmacological inhibition of NHE2 in postischemic tissues from wild-type mice also resulted in significant reductions in TER. Mucosa from NHE2(-/-) mice displayed a shift of occludin and claudin-1 expression to the Triton-X-soluble membrane fractions and showed disruption of occludin and claudin-1 localization patterns following injury. This was qualitatively and quantitatively recovered in NHE2(+/+) mice compared with NHE2(-/-) mice by the end of the 3-h recovery period. Serine phosphorylation of occludin and claudin-1 was downregulated in NHE2(-/-) postischemia compared with wild-type mice. These data indicate an important role for NHE2 in recovery of barrier function in mice via a mechanism involving tight junctions.
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