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.
journal_name
Dig Dis Scijournal_title
Digestive diseases and sciencesauthors
Siddique I,Khan Idoi
10.1023/a:1025503318409subject
Has Abstractpub_date
2003-09-01 00:00:00pages
1832-8issue
9eissn
0163-2116issn
1573-2568journal_volume
48pub_type
杂志文章abstract:BACKGROUND:Improved survival with chronic liver disease (CLD) and increased incidence in the older has led to a rapidly expanding population which faces similar "geriatric syndromes" as the general population. With risk factors such as autonomic dysfunction, cognitive impairment, and muscle abnormalities in CLD it is e...
journal_title:Digestive diseases and sciences
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更新日期:1995-01-01 00:00:00
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