| First Author | Hino K | Year | 2014 |
| Journal | PLoS One | Volume | 9 |
| Issue | 2 | Pages | e88048 |
| PubMed ID | 24498426 | Mgi Jnum | J:305044 |
| Mgi Id | MGI:6243299 | Doi | 10.1371/journal.pone.0088048 |
| Citation | Hino K, et al. (2014) Increased susceptibility to dextran sulfate sodium-induced colitis in the endoplasmic reticulum stress transducer OASIS deficient mice. PLoS One 9(2):e88048 |
| abstractText | OASIS is a basic leucine zipper (bZIP) transmembrane transcription factor that is activated in response to endoplasmic reticulum (ER) stress. Previously, we showed that OASIS regulates final maturation of goblet cells in the large intestine. In the present study, to elucidate the roles of OASIS under pathophysiological conditions, we examined the stress response and inflammatory responses in Oasis deficient (Oasis(-)/(-)) mice exposed to dextran sulfate sodium (DSS) to induce colitis. A significant loss of body weight and an increase of mortality were observed in Oasis(-)/(-) mice with DSS-induced colitis compared with those in WT mice. The mucosa of the large intestine in Oasis(-)/(-) mice exhibited severe damage involving inflammatory cell infiltration. The expression levels of ER stress and apoptosis markers in intestinal epithelial cells were upregulated in Oasis(-)/(-) mice. These abnormalities were improved by treatment with tauroursodeoxycholic acid, a chemical chaperone that facilitates protein folding. Taken together, our findings demonstrate that OASIS plays important roles in protection of the large intestinal mucosa in DSS-induced colitis through attenuation of ER stress and inflammation. |
