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Gastric Epithelium (gastric + epithelium)
Selected AbstractsGli3 null mice display glandular overgrowth of the developing stomachDEVELOPMENTAL DYNAMICS, Issue 4 2005Jae H. Kim Abstract The role of the Hedgehog signaling pathway in various aspects of gut development is still poorly understood. In the developing stomach, Sonic (Shh) and Indian (Ihh) hedgehog are expressed in both distinct and overlapping regions. Loss of Sonic hedgehog function in the stomach results in a glandular phenotype of intestinal transformation and overgrowth. These changes are reminiscent of the pre-malignant lesion, intestinal metaplasia. To determine the role of Hedgehog-related transcription factors, Gli2 and Gli3, in Shh signaling during stomach development, we conducted a mutant analysis of glandular stomach from Shh, Gli2, and Gli3 mutant mice. Although Gli2 principally mediates the activator function of Shh, surprisingly we observed minimal changes in glandular development in the Gli2 mutant stomach. Furthermore, Gli3, which typically functions as a repressor of Hedgehog signal, showed a striking phenocopy of the glandular expansion and intestinal transformation found in Shh mutant stomach. A reduction in apoptotic events was seen in all mutant stomachs with no appreciable changes in proliferation. Both Shh and Gli3 mutant stomachs displayed early changes of intestinal transformation but these did not impact on the overall differentiation of the gastric epithelium. Interestingly, the observation that Gli3 shares a similar glandular phenotype to Shh mutant stomach reveals a possible novel role of Gli3 activator in the developing stomach. The embryonic stomach is a unique model of the Hedgehog pathway function and one that may help to uncover some of the mechanisms underlying the development of intestinal metaplasia. Developmental Dynamics 234:984,991, 2005. © 2005 Wiley-Liss, Inc. [source] SOLITARY PEDUNCULATED GASTRIC GLAND HETEROTOPIA TREATED BY ENDOSCOPIC POLYPECTOMY: REPORT OF A CASEDIGESTIVE ENDOSCOPY, Issue 1 2001Kazuo Kitabayashi The patient, a 68-year-old woman with a long-standing history of schizophrenia, was admitted to our hospital complaining of vomiting which had lasted approximately 3 weeks. Endoscopic examination of the stomach revealed a solitary pedunculated submucosal tumor, of approximately 2 cm in diameter, on the anterior wall of the upper body, close to the greater curvature. The lesion was endoscopically excised using a polypectomy snare without any complication. Microscopic examination was compatible with the diagnosis of gastric gland heterotopia showing submucosal proliferation of pseudopyloric glands, fundic glands and foveolar epithelium with fibromuscular stromal framework. The proliferating foveolar epithelium and fibromuscular stroma were in continuity with the overlaying gastric mucosa and muscularis mucosae, respectively. The lesion was entirely covered by normal gastric epithelium. No atypical cells were revealed in the lesion. The clinical significance of gastric gland heterotopia is unclear because of its controversial histogenesis and carcinogenetic potential. We herein report a rare case of solitary pedunculated gastric gland heterotopia with some review of scientific reports. [source] Immunohistochemical localization of cytochrome P4501A induced by 3,3,,4,4,,5-pentachlorobiphenyl (PCB 126) in multiple organs of northern leopard frogs, Rana pipiensENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 1 2001Yue-Wern Huang Abstract Monoclonal antibody 1 12,3(MA1 12,3)recognizesanepitopeexclusivetocytochromeP450sinsubfamily1A (CYP1A) from all vertebrates tested so far, including one amphibian species. In this study, we first tested the utility of MAb 1,12-3 for detection of presumed CYP1A proteins in hepatic microsomes of northern leopard frogs treated without or with 3,3,,4,4,,5-pentachlorobiphenyl (PCB 126). Statistical analysis showed that ethoxyresorufin- O -deethylase (EROD) activities and CYP1A equivalents in treated groups were significantly increased at doses >2.3 mg/kg compared with the control groups (p < 0.05), and the increases were maintained for at least four weeks. This result confirmed that MAb 1,12-3 can be used for detection of CYP1A in northern leopard frogs and indicated that CYP1A is the primary catalyst for EROD in this species. In a subsequent experiment, sections of organs of PCB 126-treated frogs were immunohistochemically stained with MAb 1,12-3 to identify localization of the CYP1A in different cell types. The CYP1A staining was seen prominently in hepatocytes and epithelium of nephronic duct, while capillaries close to gastric epithelium and submucosal vascular epithelium in both stomach and intestine exhibited moderate to strong staining. The CYP1A was immunodetected in coronary endothelium and the vascular endothelium of lung and gonad. In skin, mild staining was seen in epithelial cells of mucous glands and serous glands and in vascular endothelium, demonstrating induction of CYP1A in the dermal layer. [source] Attack and defence in the gastric epithelium , a delicate balanceEXPERIMENTAL PHYSIOLOGY, Issue 4 2007Rod Dimaline The gastric epithelium is a complex structure formed into tubular branched gastric glands. The glands contain a wide variety of cell types concerned with the secretion of hydrochloric acid, proteases, mucus and a range of signalling molecules. All cell types originate from stem cells in the neck region of the gland, before migrating and differentiating to assume their characteristic positions and functions. Endocrine and local paracrine mediators are of crucial importance for maintaining structural and functional integrity of the epithelium, in the face of a hostile luminal environment. The first such mediator to be recognized, the hormone gastrin, was identified over a century ago and is now established as the major physiological stimulant of gastric acid secretion. Recent studies, including those using mice that overexpress or lack the gastrin gene, suggest a number of previously unrecognized roles for this hormone in the regulation of cellular proliferation, migration and differentiation. This review focuses on the identification of hitherto unsuspected gastrin-regulated genes and discusses the paracrine cascades that contribute to the maintenance of gastric epithelial architecture and secretory function. Helicobacter infection is also considered in cases where it shares targets and signalling mechanisms with gastrin. [source] Mode of attachment and lesions associated with trypanorhynch cestodes in the gastrointestinal tracts of two species of sharks collected from coastal waters of BorneoJOURNAL OF FISH DISEASES, Issue 7 2006J D Borucinska Abstract Lesions associated with two species of tapeworms within the digestive tract of wild-caught specimens of the bull shark, Carcharhinus leucas, and the sicklefin weasel shark, Hemigaleus microstoma, from Malaysian Borneo are described. Portions of the glandular stomach and pyloric gut with parasites were removed and fixed in 10% formalin buffered in sea water. Whole mounts, histological sections of tissues with and without worms in situ, and scanning electron microscopy images of detached worms were examined. Both species of cestodes belonged to the trypanorhynch family Tentaculariidae. Heteronybelinia estigmena was found in large numbers parasitizing the pyloric gut of C. leucas; an unidentified tentaculariid was found in relatively small numbers in both the glandular stomach and pyloric gut of H. microstoma. Both species burrowed their scoleces deeply in the mucosa and attached via hooked tentacles and unciniform microtriches of the scolex. The lesions induced by the parasites were marked in both sharks and ranged from acute necrotizing to chronic granulomatous gastroenteritis. Regenerative hyperplasia and intestinal metaplasia of gastric epithelium were also present. The severity and character of pathology was causally linked to the intensity of infection, the attachment mode of the parasites, and to the anatomophysiological relationships within the gut of the host shark. [source] Gene expression of AGS cells stimulated with released proteins by Helicobacter pyloriJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 4 2008Nayoung Kim Abstract Background and Aim:, Interactions between released proteins by Helicobacter pylori (H. pylori) and the cells of gastric epithelium to which it adheres may contribute to gastric inflammation and epithelial damage. The present study was performed to evaluate the gene expression of AGS gastric cancer cells stimulated with released proteins by H. pylori. Methods:, Gene expression of AGS cells to the stimulation by H. pylori -released proteins (G27 strain) were monitored using oligonucleotide microarrays. Results:, Eighty-eight genes (0.88%) and eight genes (0.08%) were up- or downregulated, respectively, by treating AGS cells with H. pylori -released proteins but not by H. pylori adhesion after 12 h of coculture. Out of the selected 40 up- and five downregulated genes, 29 upregulated genes classified as general RNA polymerase II transcription factor activity (GTF2B, PPARGC1A), SH3/SH2 adaptor activity (CRKL), transferase activity (ACLY, CRKL, PIGC, PLK4), and oxidoreductase activity (IDH1) were confirmed to be upregulated by released proteins and not by H. pylori adhesion by real-time reverse transcription,polymerase chain reaction. When the concentrated H. pylori -cultured supernatant prepared by our protocol was treated by boiling, the upregulations of 26 of these 29 genes (89.7%) except for CD160, ZNF268, and PSAT1 disappeared. This confirmed that most of these upregulations were caused by released proteins. Conclusion:, Host genes involving transcription, signaling and stress are significantly modulated by the proteins released by H. pylori. This might strengthen the gastroduodenal pathogenesis induced by H. pylori. [source] Overexpression of S100A4 is closely related to the aggressiveness of gastric cancerAPMIS, Issue 5 2003YONG GU CHO Elevated levels of the calcium-binding protein S100A4 cause metastasis of benign rat mammary tumor cells. To investigate whether S100A4 plays an important role in the invasion and metastasis of gastric cancers, we examined the gene mutations in the coding regions and expression patterns of the S100A4 in gastric adenocarcinoma in Korea. Moderate to strong expression of S100A4 was found in 53 (68.8%) of the 77 gastric adenocarcinomas, whilst normal gastric epithelium either failed to stain or showed weak staining. Interestingly, S100A4 expression was more frequently observed in gastric cancer patients with advanced gastric cancer (p=0.039), positive lymph node metastasis (p=0.001), and peritoneal dissemination (p=0.022). No gene mutations were found in the analyzed genomic area in 77 gastric adenocarcinomas and 15 gastric cancer cell lines. We found one single nucleotide polymorphism without an amino acid change, A99G, in two cases. These data suggest that the overexpression of S100A4 may be closely related to the aggressiveness of gastric cancer in Korea. [source] Study of p53 immunostaining in the gastric epithelium of cagA-positive and cagA-negative Helicobacter pylori gastritisCANCER, Issue 3 2002Ming Teh M.D. Abstract BACKGROUND p53 mutations are an early event in the multistep progression of gastric carcinoma. These mutations are often present in dysplastic and intestinal metaplastic gastric epithelium. However, the presence of immunohistochemically detectable p53 protein and p53 mutations in nondysplastic/nonmetaplastic gastric mucosa is more controversial. Recent reports have suggested that immunohistochemically detectable p53 protein may be present in the gastric epithelium of Helicobacter pylori gastritis. Furthermore, because cagA-positive H. pylori is associated with greater mucosal injury but decreased apoptosis, it would be interesting to determine if this phenotype is associated with greater immunostaining of p53, as the wild-type p53 gene helps to initiate apoptosis. METHODS One hundred thirty-five patients with H. pylori -associated gastritis were immunohistochemically stained for p53 and quantified for the extent and intensity of the staining using a semiquantitative method (0, nil staining; 6, extensive and strong staining). The cagA status of the organism was determined by Western blot. RESULTS Thirty-one patients (23%) showed strong p53 staining (, 4 of 6) in inflamed but otherwise normal gastric epithelium. In the 123 cagA-positive H. pylori gastritis patients, the average p53 staining score was 2.5 of 6. This is significantly higher than the corresponding score of 1.7 of 6 observed in the 12 patients with cagA-negative H. pylori gastritis (P = 0.04). CONCLUSIONS Our results indicate that p53 protein is immunohistochemically detectable even before gastric metaplastic/dysplastic change occurs. The results also suggest that cagA-positive H. pylori might be associated with greater p53 immunohistochemical staining. This would indicate that p53 immunohistochemical staining does not reliably differentiate between gastric dysplasia and reactive inflammatory atypia. If the p53 protein detected is a consequence of mutation, this would help to explain why cagA-positive H. pylori gastritis is associated with decreased apoptosis. Cancer 2002;95:499,505. © 2002 American Cancer Society. DOI 10.1002/cncr.10697 [source] Immunohistochemical diagnosis of the cagA -gene genotype of Helicobacter pylori with anti-East Asian CagA-specific antibodyCANCER SCIENCE, Issue 4 2007Tomohisa Uchida Cytotoxin-associated antigen A (CagA) protein produced by Helicobacter pylori is proposed to be associated with the pathogenesis of gastric cancer as well as gastritis and gastroduodenal ulcer. It has been reported that the CagA of H. pylori widespread in East Asian countries, where the mortality rate due to gastric cancer is high, is structurally different from that in Western countries, where the gastric cancer mortality rate is relatively low. In this study, we generated an antibody, East Asian CagA-specific antibody (,-EAS Ab), which is specifically immunoreactive with East Asian CagA but not with Western CagA. The CagA was immunohistochemically detected at the surface of the gastric mucosa. Interestingly, positive immunoreactivity was also detected in the nucleus and cytoplasm of the infected gastric epithelium, suggesting that CagA may play some pathogenic role in both the nucleus and cytoplasm. Immunohistochemistry of 47 gastric biopsy specimens detected East Asian CagA-positive H. pylori in 43 cases. In 46 of the 47 cases examined, the data obtained by immunohistochemistry were completely consistent with those obtained by sequencing of the cagA gene of the isolated strain, suggesting that our immunohistochemical method is reliable and useful for diagnosis of the cagA genotype. (Cancer Sci 2007; 98: 521,528) [source] Influence of polymorphisms in the NOD1/CARD4 and NOD2/CARD15 genes on the clinical outcome of Helicobacter pylori infectionCELLULAR MICROBIOLOGY, Issue 7 2006Philip Rosenstiel Summary Host immune response influences the clinical outcome of Helicobacter pylori infection leading to ulcer disease, gastric carcinoma and mucosa-associated lymphoid tissue (MALT) lymphoma. A genetic risk profile for gastric cancer has been identified, but genetic susceptibility to develop MALT lymphoma is still unclear. We investigated the role of NOD1 and NOD2 as intracellular recognition molecules for pathogen-associated molecules in H. pylori infection in vitro and analysed the influence of single nucleotide polymorphisms on susceptibility to ulcer disease and MALT lymphoma. Expression of NOD1 and NOD2 significantly sensitized HEK293 cells to H. pylori -induced NF-,B activation in a cag pathogenicity island (cagPAI)-dependent manner. In cells carrying the Crohn-associated NOD2 variant R702W the NF-,B response was significantly diminished. NOD1/NOD2 expression levels were induced in the gastric epithelium in H. pylori -positive patients. No mutations were found to be associated with gastritis or gastric ulcer development. However, the R702W mutation in the NOD2/CARD15 gene was significantly associated with gastric lymphoma. Carrier of the rare allele T had a more than doubled risk to develop lymphoma than controls [odds ratio (OR): 2.4, 95% confidence interval (CI): 1.2,4.6; P < 0.044]. H. pylori -induced upregulation of NOD1 and NOD2 in vivo may play a critical role in the recognition of this common pathogen. A missense mutation in the leucine-rich region of CARD15 is associated with gastric lymphoma. [source] | |||||||||||||