کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
105764 161519 2009 9 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Angiotensin II-generating enzymes, angiotensin-converting enzyme (ACE) and mast cell chymase (CMA1), in gastric inflammation may be regulated by H. pylori and associated cytokines
موضوعات مرتبط
علوم پزشکی و سلامت پزشکی و دندانپزشکی پزشکی قانونی
پیش نمایش صفحه اول مقاله
Angiotensin II-generating enzymes, angiotensin-converting enzyme (ACE) and mast cell chymase (CMA1), in gastric inflammation may be regulated by H. pylori and associated cytokines
چکیده انگلیسی

SummaryBackgroundThe local angiotensin II system (LAS) has numerous functions, including the regulation of growth and differentiation in the gastrointestinal tract. Angiotensin II (AngII) may be generated by angiotensin-I-converting enzyme (ACE) or mast cell chymase (CMA1) and plays an important role in inflammatory processes, although opinions differ as to which AngII-generating enzyme is primarily associated with AngII-mediated effects. ACE inhibitors have been shown to have a protective or healing effect on gastric ulcers and colitis in animal models, which could be related to the local expression of ACE.MethodsThe localisation of ACE and CMA1 was examined immunohistochemically in Helicobacter pylori gastritis, non-H. pylori gastritis, gastric ulcers and non-lesional gastric tissues. Using real-time qRT-PCR, ACE- and CMA1-mRNA expression in gastric cell lines were examined and changes in ACE levels after exposure to H. pylori or cytokines (IL-1β, IL-6, IL-8, TNFα, TGFβ1) were quantified.ResultsACE and CMA1 were not expressed in the non-lesional foveolar epithelium. Cytoplasmic staining for ACE in fundic chief cells, and apical membranous expression of ACE in the mucin-secreting cells of the antral and pyloric region was observed. ACE was found in endothelial cells of the gastric ulcer granulation tissue and CMA1 was strongly expressed in mast cells. ACE but not CMA1 was expressed in the MKN28, N87 and MKN45 gastric cell lines, and ACE mRNA expression was regulated by both H. pylori and the cytokines.ConclusionsACE in the gastric mucosa and the microvasculature of granulation tissue may represent a novel therapeutic target for the promotion of healing processes in gastritis and ulceration using ACE inhibitors or AT1R antagonists.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Pathology - Volume 41, Issue 5, August 2009, Pages 419-427