Multipotency of clonal cells derived from swine periodontal ligament and differential regulation by fibroblast growth factor and bone morphogenetic protein.
OBJECTIVE
A blood supply is indispensable for the regeneration of damaged or lost periodontal ligament (PDL) tissue. Mesenchymal stem cell-like activity of cells derived from the PDL has been identified by their capacity to form fibrous and osseous tissue and cementum. However, it remains to be clarified whether the cells have an ability to build the capillary network of blood vessels. This study evaluated the potential of cells derived from the PDL to construct a blood vessel-like structure and examined how growth factors controlled the multipotency of the cells.


METHODS
The ability of a swine PDL fibroblast cell line, TesPDL3, to construct a blood vessel-like structure was evaluated on and in the self-assembling peptide scaffold, PuraMatrix(TM). In addition, the ability of the cells to form mineralized nodules was evaluated on type I collagen-coated plastic plates. In some cases, fibroblast growth factor (FGF)-2 and bone morphogenetic protein (BMP)-2 were added to these cultures. The status of the expression of vascular and osteoblastic cell-specific markers in the cells was evaluated using reverse transcriptase-polymerase chain reaction (RT-PCR), Western blotting and immunofluorescence analyses.


RESULTS
The TesPDL3 cells not only formed mineralized nodules in response to BMP-2 stimulation but also constructed tube-like structures in response to FGF-2 stimulation. Intriguingly, FGF-2 inhibited the BMP-2-induced formation of mineralized nodules. Conversely, BMP-2 inhibited the FGF-2-induced formation of tube-like structures.


CONCLUSIONS
Periodontal ligament fibroblasts have the potential to differentiate not only into osteoblastic but also into vascular cell lineages. The destiny of the cells was reciprocally regulated by BMP-2 and FGF-2.
Shirai
K
K
Division of Periodontology and Endodontology, Department of Oral Rehabilitation, School of Dentistry, Health Sciences University of Hokkaido, 1757 Kanazawa Ishikari-Tobetsu, Hokkaido, Japan.
Ishisaki
A
A
Kaku
T
T
Tamura
M
M
Furuichi
Y
Y
D000818:Animals; D055396:Bone Morphogenetic Protein 2 / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D002113:Calcification, Physiologic / Q000187:drug effects* / Q000502:physiology; D018929:Cell Culture Techniques; D002454:Cell Differentiation / Q000187:drug effects*; D002460:Cell Line; D002999:Clone Cells / Q000166:cytology / Q000187:drug effects; D004730:Endothelium, Vascular / Q000166:cytology / Q000187:drug effects; D016222:Fibroblast Growth Factor 2 / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D005347:Fibroblasts / Q000166:cytology / Q000187:drug effects; D059630:Mesenchymal Stem Cells / Q000187:drug effects*; D039902:Multipotent Stem Cells / Q000187:drug effects*; D009130:Muscle, Smooth / Q000166:cytology / Q000187:drug effects; D018919:Neovascularization, Physiologic / Q000187:drug effects* / Q000502:physiology; D010006:Osteoblasts / Q000166:cytology / Q000187:drug effects; D010513:Periodontal Ligament / Q000166:cytology*; D051906:Smad7 Protein / Q000502:physiology; D034421:Sus scrofa; D054457:Tissue Scaffolds
D055396:Bone Morphogenetic Protein 2; D051906:Smad7 Protein; D016222:Fibroblast Growth Factor 2