Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 463, Issue 3, Pages 280-284Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2015.05.051
Keywords
Keratocystic odontogenic tumors; Knockout mouse; Smad4; Hh signaling pathway
Categories
Funding
- National Natural Science Foundation of China [81030018, 30872900, 81241062, 81200762]
- National Basic Research Program of China [2012CB966904]
- Doctoral Fund of Ministry of Education of China [20120001110043]
- Science Foundation of the Third Dental Center, Peking University School and Hospital of Stomatology [011401]
Ask authors/readers for more resources
Keratocystic odontogenic tumors (KCOTs) are cystic epithelial neoplasms with a high recurrence rate. The molecular mechanisms underlying the initiation and progression of KCOTs are still largely unknown. Previous research showed that specific ablation of Smad4 in odontoblasts and dental epithelia resulted in spontaneous KCOTs in mice, and that constitutively activated Hedgehog (Hh) signaling was detected in the cyst epithelia of both Smad4(Co/Co) OC-Cre and Smad4(Co/Co) K5-Cre mice. Here, we ablated Smad4 in mouse odontoblasts and dental epithelia and compared the sizes and numbers of KCOTs. Both the number and size of KCOTs in Smad4(Co/Co) OC-Cre mice were larger than those in Smad4(Co/Co) K5-Cre mice, suggesting that paracrine signals from root odontoblasts play a more important role than those from Hertwig's epithelial root sheath (HERS) cells. (C) 2015 Elsevier Inc. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available