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

We examined localization of extracellular signal regulated kinases (Erk) 1 and 2, and c-fos mRNA expression in normal and ulcerated gastric mucosa in rats at 1, 3 and 7 days after gastric ulcer induction. In normal gastric mucosa immunofluorescence signal for Erk-1 and Erk-2 was detectable in surface epithelial, neck and some glandular cells. In gastric mucosa of the ulcer margin, almost all epithelial cells displayed strong Erk-1 and Erk-2 immunoreactivity in the basolateral membranes and the cytoplasm. In addition 19+/-3% of cells showed nuclear localization of the Erk-1 and -2 signal. The c-fos mRNA expression was increased by 790+/-14% and 220+/-10%, respectively in gastric ulcer at 3 and 7 days after ulcer induction. Since in in vitro models nuclear translocation of Erk-1 and -2 triggers cell proliferation, our finding indicates relevance of this mechanism to gastric ulcer healing.
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PMID:Translocation of MAP (Erk-1 and -2) kinases to cell nuclei and activation of c-fos gene during healing of experimental gastric ulcers. 1006 90

It is well known that stress affects the central nervous system (CNS), neuroendocrinoimmune system and other peripheral organs such as the gastrointestinal tract. However, the process of adaptation or recovery after acute stress reactions in these systems or organs during prolonged stress has not yet been adequately investigated. To clarify the process of adaptation or recovery in these systems and organs after acute stress reactions, the time course of these responses during a single long-duration restraint stress (RTS) was studied. The expression of c-fos in the hypothalamic paraventricular nucleus (PVN) region of the brain was induced and reached a peak at 0.5 hours for c-fos mRNA and 4 hours for c-fos protein (Fos), but disappeared at 2 hours for mRNA and 16 hours for Fos during continuous RTS. The activation of the hypothalamic-pituitary-adrenal (HPA) axis during stress resulted in rapid increases in the plasma levels of adrenocorticotropic hormone (ACTH) and corticosterone (CORT). Whereas the increase in ACTH was transient, the rise in CORT was maintained throughout the duration of the stress. A rapid significant decrease after stress exposure and following a slow and complete or partial recovery were observed in a number of total white blood cells (WBC), lymphocytes (LYM), helper T cells (Th) and cytotoxic/suppressor T cells (CTL/Ts). A gastric ulcer was found in 1/6 and 6/6 rats at 8 hours and 16 hours RTS, respectively. These results suggest that adaptive changes may occur in c-fos expression in the PVN, ACTH release and immune response, but not for CORT release, following acute stress reaction during long-duration RTS. In addition, any associated organic damage, such as gastric ulceration, was also suggested to possibly be progressive according to the duration of RTS.
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PMID:PVN c-fos expression, HPA axis response and immune cell distribution during restraint stress. 1206 82

The maintenance of gastric mucosal function and integrity highly depends on the status of microcirculation. Vasoactive agents--prostaglandins, nitric oxide and sensory neuropeptides (e.g. calcitonin gene-related peptide)--play a crucial role in mucosal defensive processes. Beside the local release of vasoactive mediators the central nervous system is also involved in regulation of gastric functions. Cerebral lesions, stimulation of different brain areas can result in gastric mucosal injury. Noxious challenge of gastric mucosa alters the sodium currents in gastric sensory neurons and induces cfos mRNA expression in nucleus tractus solitarii and area postrema. Vagal nerve has long been established to play a permissive role in the development of gastric lesions. However, several lines of evidences suggest its physiological relevance in the enhancement of gastric mucosal resistance. It was concluded that gastroprotection can be induced by low level of central vagal stimulation and the consequent release of prostaglandins, nitric oxide, and calcitonin gene-related peptide. Prostaglandins, nitric oxide and sensory neuropeptides play a role also in ulcer healing by stimulating the formation of growth factors, the epithelial proliferation and angiogenesis. Both systemic and local administration of growth factors accelerated the ulcer healing. Local, single injection of plasmid-DNA encoding vascular endothelial growth factor (VEGF) was shown to stimulate the ulcer healing in the rat. The transient, local expression of VEGF in ulcerated tissue might be a new therapeutic strategy in the treatment of gastric ulcer disease.
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PMID:Gastric mucosal protection: from prostaglandins to gene-therapy. 1563 36

On the basis of its temporal and spatial pattern of expression during the healing of gastric ulcers, RegI is implied to be a key growth factor governing the gastric progenitor cell proliferation, which is fundamental for reconstruction of the gastric tissue; however, there is no direct in vivo evidence. The aim of this study was to use RegI-transgenic (Tg) mice to test the role of RegI protein in the healing of experimentally induced gastric ulcers. The stomachs from 48 pairs of wild-type (Wt) and Tg littermates were examined for gastric erosions after 24 h of water-immersion stress, or, 6, 12, 18 and 24 h after oral administration of HCl/ethanol. Expression levels of c-fos and c-myc proto-oncogenes were examined over time by real-time reverse transcriptase PCR to assess gastric cell proliferation. Almost all the littermate pairs tested showed superiority of Tg mice over Wt mice in the ability of decreasing ulcer index (UI) (cumulative length of erosion). The time-course study revealed that the UIs of Tg were lower in the healing phase, and not in the injury phase. The fraction of proliferating cells was higher in Tg mice than in Wt mice throughout the time course as assessed by c-fos expression levels. This is the first in vivo evidence that RegI has a role in gastric ulcer healing. We suggest that RegI exerts its effects by promoting growth and not by cytoprotection.
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PMID:In vivo evidence for the role of RegI in gastric regeneration: transgenic overexpression of RegI accelerates the healing of experimental gastric ulcers. 2015 93