| First Author | Lo Sasso G | Year | 2014 |
| Journal | PLoS One | Volume | 9 |
| Issue | 7 | Pages | e102495 |
| PubMed ID | 25013930 | Mgi Jnum | J:219037 |
| Mgi Id | MGI:5619274 | Doi | 10.1371/journal.pone.0102495 |
| Citation | Lo Sasso G, et al. (2014) Loss of Sirt1 function improves intestinal anti-bacterial defense and protects from colitis-induced colorectal cancer. PLoS One 9(7):e102495 |
| abstractText | Dysfunction of Paneth and goblet cells in the intestine contributes to inflammatory bowel disease (IBD) and colitis-associated colorectal cancer (CAC). Here, we report a role for the NAD+-dependent histone deacetylase SIRT1 in the control of anti-bacterial defense. Mice with an intestinal specific Sirt1 deficiency (Sirt1int-/-) have more Paneth and goblet cells with a consequent rearrangement of the gut microbiota. From a mechanistic point of view, the effects on mouse intestinal cell maturation are mediated by SIRT1-dependent changes in the acetylation status of SPDEF, a master regulator of Paneth and goblet cells. Our results suggest that targeting SIRT1 may be of interest in the management of IBD and CAC. |
