Inactivation of Fam20C in cells expressing type I collagen causes periodontal disease in mice.

Bibliographic Details
Title: Inactivation of Fam20C in cells expressing type I collagen causes periodontal disease in mice.
Authors: Peihong Liu, Hua Zhang, Chao Liu, Xiaofang Wang, Li Chen, Chunlin Qin
Source: PLoS ONE, Vol 9, Iss 12, p e114396 (2014)
Publisher Information: Public Library of Science (PLoS), 2014.
Publication Year: 2014
Collection: LCC:Medicine
LCC:Science
Subject Terms: Medicine, Science
More Details: FAM20C is a kinase that phosphorylates secretory proteins. Previous studies have shown that FAM20C plays an essential role in the formation and mineralization of bone, dentin and enamel. The present study analyzed the loss-of-function effects of FAM20C on the health of mouse periodontal tissues.By crossbreeding 2.3 kb Col 1a1-Cre mice with Fam20Cfl/fl mice, we created 2.3 kb Col 1a1-Cre;Fam20Cfl/fl (cKO) mice, in which Fam20C was inactivated in the cells that express Type I collagen. We analyzed the periodontal tissues in the cKO mice using X-ray radiography, histology, scanning electron microscopy and immunohistochemistry approaches.The cKO mice underwent a remarkable loss of alveolar bone and cementum, along with inflammation of the periodontal ligament and formation of periodontal pockets. The osteocytes and lacuno-canalicular networks in the alveolar bone of the cKO mice showed dramatic abnormalities. The levels of bone sialoprotein, osteopontin, dentin matrix protein 1 and dentin sialoprotein were reduced in the Fam20C-deficient alveolar bone and/or cementum, while periostin and fibrillin-1 were decreased in the periodontal ligament of the cKO mice.Loss of Fam20C function leads to periodontal disease in mice. The reduced levels of bone sialoprotein, osteopontin, dentin matrix protein 1, dentin sialoprotein, periostin and fibrillin-1 may contribute to the periodontal defects in the Fam20C-deficient mice.
Document Type: article
File Description: electronic resource
Language: English
ISSN: 1932-6203
Relation: http://europepmc.org/articles/PMC4257665?pdf=render; https://doaj.org/toc/1932-6203
DOI: 10.1371/journal.pone.0114396
Access URL: https://doaj.org/article/83c937a0a745456387675c4f5c4ba383
Accession Number: edsdoj.83c937a0a745456387675c4f5c4ba383
Database: Directory of Open Access Journals
More Details
ISSN:19326203
DOI:10.1371/journal.pone.0114396
Published in:PLoS ONE
Language:English