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

Liu P, Zhang H, Liu C, Wang X, Chen L, Qin C - PLoS ONE (2014)

Bottom Line: Previous studies have shown that FAM20C plays an essential role in the formation and mineralization of bone, dentin and enamel.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.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Periodontics, Harbin Medical University School of Stomatology, Harbin, Heilongjiang, 150001, China; Department of Biomedical Sciences and Center for Craniofacial Research and Diagnosis, Texas A&M University Baylor College of Dentistry, Dallas, Texas, 75246, United States of America.

ABSTRACT

Background: 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.

Methods: 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.

Results: 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.

Conclusion: 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.

Show MeSH

Related in: MedlinePlus

IHC analyses of periostin and fibrillin-1 in the periodontal tissues of 4-week-old mice.a1 was the higher magnification view of the box area in Figure 9a (normal mice, anti-periostin). b1 was the higher magnification view of the box area in b (cKO mice). c1 was the higher magnification view of the box area in c (normal mice, anti-fibrillin-1). d1 was the higher magnification view of the box area in d (cKO mice). Strong signals for periostin were seen in the PDL, in particular, along the collagen fibers in the normal mice (a, a1). The level of periostin in the PDL of the cKO mice was reduced (b, b1). Fibrillin-1 signals were strong in certain areas of the PDL and its signals were weaker in the PDL of cKO mice (d, d1) compared to the normal mice (c, c1). Bar in a, b, c or d: 500 µm; bar in a1, b1, c1 or d1: 100 µm.
© Copyright Policy
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4257665&req=5

pone-0114396-g009: IHC analyses of periostin and fibrillin-1 in the periodontal tissues of 4-week-old mice.a1 was the higher magnification view of the box area in Figure 9a (normal mice, anti-periostin). b1 was the higher magnification view of the box area in b (cKO mice). c1 was the higher magnification view of the box area in c (normal mice, anti-fibrillin-1). d1 was the higher magnification view of the box area in d (cKO mice). Strong signals for periostin were seen in the PDL, in particular, along the collagen fibers in the normal mice (a, a1). The level of periostin in the PDL of the cKO mice was reduced (b, b1). Fibrillin-1 signals were strong in certain areas of the PDL and its signals were weaker in the PDL of cKO mice (d, d1) compared to the normal mice (c, c1). Bar in a, b, c or d: 500 µm; bar in a1, b1, c1 or d1: 100 µm.

Mentions: In the normal mice, strong signals for periostin were observed across the PDL, with an accentuated accumulation along the thick collagen fibers (Figures 9a, 9a1). The level of periostin in the PDL of the cKO mice was dramatically reduced (Figures 9b, 9b1).


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

Liu P, Zhang H, Liu C, Wang X, Chen L, Qin C - PLoS ONE (2014)

IHC analyses of periostin and fibrillin-1 in the periodontal tissues of 4-week-old mice.a1 was the higher magnification view of the box area in Figure 9a (normal mice, anti-periostin). b1 was the higher magnification view of the box area in b (cKO mice). c1 was the higher magnification view of the box area in c (normal mice, anti-fibrillin-1). d1 was the higher magnification view of the box area in d (cKO mice). Strong signals for periostin were seen in the PDL, in particular, along the collagen fibers in the normal mice (a, a1). The level of periostin in the PDL of the cKO mice was reduced (b, b1). Fibrillin-1 signals were strong in certain areas of the PDL and its signals were weaker in the PDL of cKO mice (d, d1) compared to the normal mice (c, c1). Bar in a, b, c or d: 500 µm; bar in a1, b1, c1 or d1: 100 µm.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4257665&req=5

pone-0114396-g009: IHC analyses of periostin and fibrillin-1 in the periodontal tissues of 4-week-old mice.a1 was the higher magnification view of the box area in Figure 9a (normal mice, anti-periostin). b1 was the higher magnification view of the box area in b (cKO mice). c1 was the higher magnification view of the box area in c (normal mice, anti-fibrillin-1). d1 was the higher magnification view of the box area in d (cKO mice). Strong signals for periostin were seen in the PDL, in particular, along the collagen fibers in the normal mice (a, a1). The level of periostin in the PDL of the cKO mice was reduced (b, b1). Fibrillin-1 signals were strong in certain areas of the PDL and its signals were weaker in the PDL of cKO mice (d, d1) compared to the normal mice (c, c1). Bar in a, b, c or d: 500 µm; bar in a1, b1, c1 or d1: 100 µm.
Mentions: In the normal mice, strong signals for periostin were observed across the PDL, with an accentuated accumulation along the thick collagen fibers (Figures 9a, 9a1). The level of periostin in the PDL of the cKO mice was dramatically reduced (Figures 9b, 9b1).

Bottom Line: Previous studies have shown that FAM20C plays an essential role in the formation and mineralization of bone, dentin and enamel.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.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Periodontics, Harbin Medical University School of Stomatology, Harbin, Heilongjiang, 150001, China; Department of Biomedical Sciences and Center for Craniofacial Research and Diagnosis, Texas A&M University Baylor College of Dentistry, Dallas, Texas, 75246, United States of America.

ABSTRACT

Background: 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.

Methods: 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.

Results: 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.

Conclusion: 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.

Show MeSH
Related in: MedlinePlus