| First Author | Li F | Year | 2013 |
| Journal | Dev Dyn | Volume | 242 |
| Issue | 5 | Pages | 444-55 |
| PubMed ID | 23362225 | Mgi Jnum | J:194979 |
| Mgi Id | MGI:5475400 | Doi | 10.1002/dvdy.23933 |
| Citation | Li F, et al. (2013) Conditional expression of the dominant-negative TGF-beta receptor type II elicits lingual epithelial hyperplasia in transgenic mice. Dev Dyn 242(5):444-55 |
| abstractText | Background: The transforming growth factor-beta (TGF-beta) signaling pathway is generally believed to be a potent inhibitor of proliferation. However, many epithelia lacking the essential Tgfbr2 gene still maintain normal tissue homeostasis. Here, transgenic mice expressing rtTA from the human keratin 14 (K14) promoter were used to generate an inducible dominant-negative TGF-beta receptor type II (Tgfbr2) mutant model, which allowed us to distinguish between the primary and secondary effects of TGF-beta signaling disruption by Doxycycline treatment in K14+ epithelial stem cells. Results: We showed that in mice lacking TGF-beta signaling in K14+ cells, invasive carcinomas developed on the ventral surface of the tip of the tongue, while filiform papillae on the dorsal surface showed different pathological changes from the tip to the posterior of the tongue. In addition, acetylation levels of histone H4 and histone H3 rapidly increased, while pMAPK activity was enhanced and Jagged2 inactivated in lingual epithelia after disruption of TGF-beta signaling. Conclusions: Our results contribute to the understanding of TGF-beta signaling in regulating homeostasis and carcinogenesis in lingual epithelia. Developmental Dynamics 242:444-455, 2013. (c) 2013 Wiley Periodicals, Inc. |
