Related Experiment Video
Updated: Jul 14, 2026
Mouse Models Of Helicobacter Infection And Gastric Pathologies
Published on: October 18, 2018
Helicobacter pylori-induced changes in the gastric mucosa are associated with mitogen-activated protein kinase (MAPK)
Furuzan Kacar1, Ibrahim Meteoğlu, Hadi Yasa
1Department of Pathology, Adnan Menderes University, Aydin, Turkey.
Background:
Gastric cancers are usually associated with and preceded by Helicobacter pylori (HP) infection, gastric atrophy, intestinal metaplasia, and dysplasia. HP infection alters cell kinetics of the gastric mucosa. Both proliferation and apoptosis are increased. Proinflammatory cytokines are responsible for some of these alterations. The mitogen-activated protein kinase (MAPK) signaling pathway has been implicated as a causative factor in these alterations based on in vitro studies. In this study, we investigated the effects of HP infection on gastric mucosal proliferation, apoptotic mechanisms, and the activation status of the MAPK signaling pathway at various stages of gastric carcinogenesis, especially intestinal metaplasia and dysplasia caused by HP infection.
Design:
Stomach biopsies representing normal (n=20), HP+ (n=25), HP+ with intestinal metaplasia (n=25), HP+ with dysplasia (n=15) and gastric adenocarcinoma (n=30; 20 HP+ and 10 HP-) cases were selected. Cell proliferation was assessed by proliferating cell nuclear antigen immunostaining. Apoptosis and survival-related markers; cleaved caspase-3, and phospho-MAPK extracellular signal-regulated kinase (ERK) were detected by immunohistochemical methods.
Results:
Proliferation index (proliferating cell nuclear antigen) and cleaved caspase-3 expression were higher in the HP+, HP+ with intestinal metaplasia, and HP+ with dysplasia groups than in normal controls (P<0.05). Cleaved caspase-3 activity was also high in the adenocarcinomas. Phospho-MAPK(ERK) expression was increased in the HP+, HP+ with intestinal metaplasia, HP+ with dysplasia and adenocarcinomas compared with the normal control group. Whereas HP- gastric carcinomas had a lower expression of phospho-MAPK.
Conclusions:
HP infection increases the proliferative rate of gastric foveolar cells in conjunction with an increased apoptotic rate and activation of MAPK(ERK). MAPK activation seems to be a significant and persistent event in the HP-induced neoplastic transformation.
More Related Videos
10:44One-step Negative Chromatographic Purification of Helicobacter pylori Neutrophil-activating Protein Overexpressed in Escherichia coli in Batch Mode
Published on: June 18, 2016
11:48Mouse- and Human-derived Primary Gastric Epithelial Monolayer Culture for the Study of Regeneration
Published on: May 7, 2018
Related Concept Videos
01:26Gastritis II: Pathophysiology
01:22Pathophysiology of Peptic Ulcer Disease: Injurious Factors
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds to M3...
01:24Peptic Ulcer Disease II: Pathophysiology
01:28Peptic Ulcer Disease II: Pathophysiology
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
01:17Gastritis-II: Pathophysiology
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
01:27Peptic Ulcer