Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The finding of cytokeratin positivity in non-epithelial cells in 9/15 cases of performing or penetrating gastric ulcer is reported. Two different monoclonal anti-cytokeratin antibodies were used and both produced a strong positivity in spindle and polyglonal cells in the gastric wall. These cells were often distributed near the peritoneal surface, but they were also found in central parts of the gastric wall. The cytokeratin-positive cells had no connection with the gastric mucosa, lacked epithelial features in routinely stained sections and were not positively stained by antibodies to other epithelial markers (EMA and Ber-Ep 4). Many of the cytokeratin-positive cells were also positive for vimentin. There was no evidence of malignancy in any of the cases, but cytokeratin-positive cells like those in the present study may be erroneously interpreted as infiltrating carcinoma. The true nature of the cytokeratin-positive cells was not revealed in the present study. It is concluded that cytokeratin positivity must be evaluated with care and that it is valuable to add antibodies other than anti-cytokeratins for the recognition of epithelial cell differentiation.
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PMID:Immunoreactivity to cytokeratins in non-epithelial cells in deep gastric ulcer. 769 92

Mesenchymal stem cells (MSCs), a subpopulation of adult somatic stem cells, are an attractive stem cell source in regenerative medicine because of their multipotentiality. We examined the effects of MSC transplantation on gastric ulcer healing. Putative MSCs, isolated from bone marrow aspirates of male rats by dish adherence and expanded in culture, were characterized by flow cytometry and reverse transcription-polymerase chain reaction. Gastric ulcers were induced by serosal application of acetic acid on the anterior wall of the stomach in female rats. Either MSCs (labeled with PKH67; 1x10(7) cells) or vehicle was injected into the gastric wall surrounding the ulcer. The healing process of the ulcer and the influence of anti-vascular endothelial growth factor (VEGF) antibody were examined. CD29-positive, CD90-positive, CD34-negative, and CD45-negative MSCs expressed mRNAs for VEGF and hepatocyte growth factor (HGF). The MSCs were transplantable to the gastric tissue surrounding the ulcer, where a majority of the engrafted cells were positive for vimentin. The transplantation significantly accelerated gastric ulcer healing compared with controls. The engrafted MSCs also expressed VEGF and HGF. Administration of anti-VEGF neutralizing antibody dose dependently reduced the MSC-induced promotion of ulcer healing. In conclusion, MSC transplantation accelerated gastric ulcer healing, possibly through the induction of angiogenesis in the gastric mucosa via the secretion of VEGF. The beneficial effects of MSCs might be mediated not only by their differentiation into gastric interstitial cells, but also by their ability to supply angiogenic factors.
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PMID:Topical transplantation of mesenchymal stem cells accelerates gastric ulcer healing in rats. 1820 10

CCN1 is a matricellular protein that activates many genes related to wound healing and tissue remodeling in fibroblasts, but its effect on epithelial cells remains unclear. This study examined the role of CCN1 in epithelial wound healing using rat gastric epithelial cells and rat stomach ulcer as in vitro and in vivo models, respectively. We found that CCN1 expression is highly upregulated in the epithelial cells adjacent to a wound and remains high until the wound is healed. Upregulation of CCN1 activates a transient epithelial-mesenchymal transition in the epithelial cells at the migrating front and drives wound closure. Once the wound is healed, these epithelial cells and their progeny can resume their original epithelial phenotype. We also found that CCN1-induced E-cadherin loss is not due to transcriptional regulation but rather protein degradation due to the collapse of adherens junctions, which is contributed by beta-catenin translocation. CCN1-activated integrin-linked kinase mediates this process. Finally, our in vivo study showed that locally neutralizing CCN1 drastically impairs wound closure, whereas local injection of recombinant CCN1 protein induces expression of vimentin and smooth muscle alpha-actin in normal gastric mucosal epithelial cells and accelerates re-epithelialization during ulcer healing. In conclusion, our study indicates that CCN1 can induce reversible epithelial-mesenchymal transition, and this feature may have great value for clinical wound healing.
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PMID:CCN1 induces a reversible epithelial-mesenchymal transition in gastric epithelial cells. 2045 73