Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0022104 (irritable bowel syndrome)
 8,033 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Irritable bowel syndrome (IBS) is one of the most common functional disorders of the gastrointestinal tract. It is characterized by abdominal pain and changes in bowel habits. Various studies have investigated the pathophysiologic processes underlying IBS, but the mechanism remains poorly understood. In the present study, we established an IBS model and identified differentially expressed proteins in colon tissue of IBS rats compared with healthy controls by 2-D gel electrophoresis, MALDI-TOF-MS, and Western blot analysis. Our results showed that 13 of the 1396 protein spots on 2-D gel were differently expressed between the IBS and control groups. Ontological analysis of these proteins revealed primary roles in catalytic activity (protein disulfide-isomerase A3, glyoxalase I, cathepsin S, alpha-enolase), structural support (cytokeratin 8), antioxidant activity (peroxiredoxin-6), protein binding (transgelin, serpin peptidase inhibitor B5), and signal transduction (40S ribosomal protein SA). Protein disulfide-isomerase A3 and cytokeratin 8 overexpression in IBS were confirmed by Western blot. The findings indicate that multiple proteins are involved in IBS processes that influence intestinal tract immunity, inflammation, and nerve regulation. Our study provides useful candidate genes and proteins for further investigation.
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PMID:Proteomic analysis of colonic mucosa in a rat model of irritable bowel syndrome. 2046 17

This study investigated the mechanism of protein disulfide-isomerase A3 (PDIA3)-induced visceral hypersensitivity in irritable bowel syndrome (IBS). Rats were treated with saline (control), acetic acid and restraint stress (IBS model), empty vector (RNAi control) and PDIA3-RNAi vector (PDIA3-RNAi). Mesenteric lymph node DCs (MLNDCs) and splenic CD4+/CD8+ T cells were isolated for co-cultivation. Compared with control, MLNDCs co-cultured with CD4+ or CD8+ T cells showed an increased ability to promote T cell proliferation and produced more IL-4 or IL-9 secretion. Compared with the RNAi control, MLNDCs from the PDIA3 knockdown models were less effective in promoting the proliferation of CD4+/CD8+ T cells. It is concluded that PDIA3 plays an important role in the development of IBS through the DC-mediated activation of T cells, resulting in degranulation of MCs and visceral hypersensitivity.
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PMID:PDIA3 gene induces visceral hypersensitivity in rats with irritable bowel syndrome through the dendritic cell-mediated activation of T cells. 2789 22

This study aimed to elucidate the role of PDIA3 in visceral hypersensitivity of rats with irritable bowel syndrome (IBS). Fourty eight SD rats were randomly divided into four groups (n=12): control group, IBS-empty virus group (IBS-1), IBS-PDIA3 silence group (IBS-2), and IBS-the control group (IBS-3). Visceral hypersensitivity models were established by using acetic acid enema combined with restraint stress, and assayed by abdominal withdrawal reflexes (AWR). Mast cells (MCs) in ileocecal mucosa were counted with toluidine blue staining. Degranulation of MCs was observed under electron microscopy. Serum and mucosal levels of IL-4 and IL-9 were measured with ELISA and QT-PCR. Intestinal tryptase and PAR-2 expression was examined with ELISA and Western blot. The Results showed that PDIA3 plays an important role in the formation of visceral hypersensitivity by increasing systemic and colon mucosal expressions of IL-4 and IL-9, activating mast cells and upregulating PAR-2 expression of target organs.
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PMID:Effect of PDIA3 gene silence on colonic mast cells and visceral sensitivity of rats with irritable bowel syndrome. 3196 10