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. 2011 Oct;46(10):1177-86.
doi: 10.1007/s00535-011-0433-7. Epub 2011 Jul 13.

Expression of angiotensin II type 1 and type 2 receptor mRNAs in the gastric mucosa of Helicobacter pylori-infected Mongolian gerbils

Mitsushige Sugimoto  1 , Tomoyuki Ohno, Yoshio Yamaoka
Affiliations

Expression of angiotensin II type 1 and type 2 receptor mRNAs in the gastric mucosa of Helicobacter pylori-infected Mongolian gerbils

Mitsushige Sugimoto et al. J Gastroenterol. 2011 Oct.

Abstract

Background: The renin-angiotensin system (RAS) plays an important role in normal homeostasis, carcinogenesis-related angiogenesis, and cell proliferation. Helicobacter pylori infection causes infiltration of inflammatory cells into the gastric mucosa and is considered the major cause of gastric cancer. Whether RAS plays a role in H. pylori infection-related gastric diseases remains unclear. We investigated the changes in gastric mucosal angiotensin II type 1 receptor (AT1R) and type 2 receptor (AT2R) mRNA levels throughout the time course of H. pylori infection in Mongolian gerbils.

Methods: Mongolian gerbils were infected with wild-type H. pylori (for 12 months) or with its isogenic oipA mutant (for 3 months). Gastric mucosal AT1R and AT2R mRNA levels were assessed using real-time reverse transcription-polymerase chain reaction.

Results: The gastric mucosal AT1R mRNA level was significantly associated with the severity of inflammatory cell infiltration into the gastric mucosa that reached maximal levels at 12 months after infection in both the antrum and body. Inflammatory cell infiltration scores and AT1R and AT2R mRNA levels were significantly lower in oipA mutant than wild-type infections. Mucosal AT1R and AT2R mRNA expressions in wild-type H. pylori-infected gerbils with gastric ulcers were significantly higher than in those without ulcers (P < 0.01).

Conclusions: Gastric mucosal ATR expression gradually increases during the course of H. pylori infection. Up-regulation of the RAS in association with progressive gastric inflammation suggests a potential role of the RAS in gastric carcinogenesis. OipA appears to play a role in AT1R and AT2R expression and the resulting inflammation.

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Conflict of interest statement

Conflict of interest The authors declare no conflicts of interest.

Figures

Fig. 1
Fig. 1
Gastric antrum (white circles) and body (black squares) mucosal AT1R and AT2R mRNA levels in Mongolian gerbils infected with Helicobacter pylori strain 7.13 (wild-type) over 12 months. The maximum levels of AT1R and AT2R mRNA were seen 12 months after inoculation in both the antrum and body, except for AT2R in the antrum. Data are shown as means ± SEM. *P <0.05 compared with the antrum. AT1R angiotensin II type 1 receptor, AT2R angiotensin II type 2 receptor
Fig. 2
Fig. 2
AT1R and AT2R mRNA levels in the gastric antral (a, b) and body (c, d) mucosa of Mongolian gerbils infected with Helicobacter pylori strain 7.13 (wild-type) (white circles), Mongolian gerbils infected with oipA mutant (black triangles), and negative controls (white squares) over 3 months. Data are shown as means ± SEM. *P <0.05; compared with wild-type. AT1R angiotensin II type 1 receptor, AT2R angiotensin II type 2 receptor
Fig. 3
Fig. 3
Correlations between AT1R and AT2R mRNA levels and MNC infiltration scores in the antrum (a, b) and body (c, d). AT1R and AT2R mRNA levels were significantly correlated with the MNC infiltration score. AT1R angiotensin II type 1 receptor, AT2R angiotensin II type 2 receptor, MNC mononuclear cell
Fig. 4
Fig. 4
Correlation between AT1R and AT2R mRNA levels. AT1R mRNA levels were strongly correlated with AT2R mRNA levels. AT1R angiotensin II type 1 receptor, AT2R angiotensin II type 2 receptor
Fig. 5
Fig. 5
AT1R and AT2R levels in the antral gastric mucosa of the Mongolian gerbil ulcer group (GU+) and non-ulcer group (GU−). *P <0.05 (vs. non-ulcer group). AT1R angiotensin II type 1 receptor, AT2R angiotensin II type 2 receptor, GU gastric ulcer
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