ArticleDigestive diseases and sciences2003
Regulation of Na/H exchanger-1 in gastroesophageal reflux disease: possible interaction of histamine receptor.
Article in Digestive diseases and sciences, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Decreased NHE3 expression in colon cancer is associated with DNA damage, increased inflammation and tumor growth.Scientific reports · 2022Article
- Carbonic Anhydrases II, IX, and XII in Reflux Esophagitis.Digestive diseases and sciences · 2022Article
- Advances in research on the regulatory mechanism of NHE1 in tumors.Oncology letters · 2021Review
- The therapeutic importance of acid-base balance.Biochemical pharmacology · 2021Review
- OEsophageal Ion Transport Mechanisms and Significance Under Pathological Conditions.Frontiers in physiology · 2020Review
- (Patho-)Physiology of NaFrontiers in physiology · 2019Review
- SLC9 Gene Family: Function, Expression, and Regulation.Comprehensive Physiology · 2018Review
- Pathophysiology of Intestinal NaCellular and molecular gastroenterology and hepatology · 2017Article
- Changes in Gene Expression Patterns of Circadian-Clock, Transient Receptor Potential Vanilloid-1 and Nerve Growth Factor in Inflamed Human Esophagus.Scientific reports · 2015Article
- Article
- Focal adhesion kinase controls pH-dependent epidermal barrier homeostasis by regulating actin-directed Na+/H+ exchanger 1 plasma membrane localization.The American journal of pathology · 2007Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Na/H exchanger-1 (NHE-1) isoform regulates intracellular pH and protects the esophageal mucosa. These functions are compromised in gastroesophageal reflux disease (GERD); however, the role and the underlying mechanism of NHE-1 regulation are obscure. To address this issue, NHE-1 protein and mRNA levels were measured by ECL western blot analysis and a semiquantitative RT-PCR using alpha-actin as an internal control. Ouabain-sensitive and K-stimulated p-nitrophenylphosphatase activity was measured as a marker of the sodium pump. The level of NHE-1 protein and mRNA and sodium pump activity was increased in GERD patients with or without esophagitis. Interestingly, myeloperoxidase (MPO) activity and infiltration of inflammatory cells were significantly increased in the GERD patients with esophagitis as compared to the GERD without esophagitis and the normal controls. This induction of NHE-1 and sodium pump was reversed in the GERD patients taking an H2 blocker, but not in those taking antacids. The internal control alpha-actin did not change under these conditions. Yield of total RNA and crude microsomal proteins was also statistically similar in all the test groups. These findings demonstrate that induction of NHE-1 is regulated posttranscriptionally through a possible interaction of histamine receptor. Induction of NHE-1 and sodium pump activity together might be a mechanism underlying the GERD pathogenesis and suggests a significance of NHE-1 inhibition in the treatment of GERD.
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