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1 ile PIEZO2 was localized in odontoblasts and cementoblasts.
2 AE/KAE)) mice and OCCM.30 murine (Ibsp(KAE)) cementoblasts.
3 promoter-luciferase constructs into OCCM-30 cementoblasts.
4 the periodontium, including osteoblasts and cementoblasts.
5 clastogenesis-associated molecules in murine cementoblasts.
6 e expression in a line of immortalized mouse cementoblasts.
7 tion and exerted a proinflammatory effect on cementoblasts.
8 ) carrier + follicle cells, and 3) carrier + cementoblasts.
9 ls, including odontoblasts, osteoblasts, and cementoblasts.
10 ter SV40 transgenic mice were used to obtain cementoblasts.
11 n mRNA was found after PDGF gene delivery to cementoblasts.
12 sgenic mice were used to obtain immortalized cementoblasts.
13 gene expression in WT and Ibsp(-/-) OCCM.30 cementoblasts.
14 hat PDLCs differentiate into osteoblasts and cementoblasts.
15 nesis using: 1) OCCM-30 (immortalized murine cementoblasts), 2) RAW 264.7 cells (murine myeloid cells
16 of platelet-derived growth factor stimulates cementoblast activity that is sustained above that of rh
17 n peptide appears to have a direct effect on cementoblast activity that may prove significant during
20 investigation was to evaluate the ability of cementoblasts and dental follicle cells to promote perio
21 significantly increased the proliferation of cementoblasts and mineralized nodules at all concentrati
23 ion in expression of BSP mRNA and protein in cementoblasts and surrounding osteoblasts in comparison
24 ve Hertwig's root sheath epithelia, putative cementoblasts, and a morphologically correct enamel orga
25 rs that can give rise to mature osteoblasts, cementoblasts, and fibroblasts within the periodontium.
26 s the balance of OPG and RANKL production by cementoblasts, and further indicate that this effect, in
28 t cell types in vivo and support the role of cementoblasts as a tool to better understand periodontal
29 the apically located cellular cementum, some cementoblasts become embedded in the cementoid matrix an
31 rganic phosphate (ePi) is a key regulator of cementoblast behavior, both in vivo and in vitro, and re
34 results revealed high level transduction of cementoblasts by gene transfer for 7 days as evidenced b
35 rotein expression in the immortalized murine cementoblast cell line OCCM-30 after treatment with chem
42 PR-deficient progenitors exhibit accelerated cementoblast differentiation with upregulation of nuclea
46 of prior in situ studies, OC is expressed by cementoblasts during root development, but not by cells
47 achment protein (CAP), and recently reported cementoblast-enriched genes, secreted frizzled related p
50 roles of the chemerin/ChemR23 interaction in cementoblast function and IRR and reveal a new IRR thera
51 These findings further our understanding of cementoblast function and suggest that differentially in
52 ngs suggest that nicotine negatively affects cementoblast function and the formation of new cementum,
56 showed that the mineralized tissue formed by cementoblasts gave strong signals for both BSP and OCN g
63 lture conditions, PDLSCs differentiated into cementoblast-like cells, adipocytes, and collagen-formin
66 contrast, in defects treated with carrier + cementoblasts, mineralized tissues were noted at the hea
67 rs using collagenase/trypsin digestion, only cementoblasts, not PDL cells, are immortalized and thus,
68 on of PDL stem cells committed to osteoblast/cementoblast (O/C) differentiation remains to be elucida
69 ition to expression of genes associated with cementoblasts, OC/CM cells promoted mineral nodule forma
72 the effects of nicotine on the functions of cementoblasts (OCCM-30) in terms of proliferation, migra
73 , a clonal population of immortalized murine cementoblasts (OCCM-30) was exposed to full-length murin
79 to odontoblasts but also to cementum-forming cementoblasts of the elongating root, while showing plas
80 PDL cells (PDLCs), on top of osteoblasts and cementoblasts on the surface of alveolar bone and cement
83 in [OCN], and osteopontin [OPN], markers for cementoblast/osteoblast maturation/mineralization), von
84 SMA9 cells expanded, and differentiated into cementoblasts, osteoblasts, and periodontal ligament fib
87 ) to inactivate Piezo1 in mature osteoblasts/cementoblasts, osteocytes/cementocytes, and odontoblasts
89 LRAP, and the proliferation and migration of cementoblast/periodontal ligament cells by LRAP and P172
90 wild-type (WT) osteoclast progenitor and KO cementoblast/periodontal ligament cells displayed more t
91 Proliferation and migration rates of the KO cementoblast/periodontal ligament cells were lower than
95 -1) , 1, 2.5, 5, and 10 mM) of nicotine, and cementoblast proliferation was then evaluated using a re
97 profile, and biomineralization potential of cementoblasts suggesting that such factors alone or in c
98 e evaluated the efficacy of RvD1 and RvE1 on cementoblasts, the key cells involved in dental cementum
99 hosphate regulates OPN gene transcription in cementoblasts through a pathway that requires a function
103 ortions of the implants in two of the 6-week cementoblast-treated specimens, possibly due in part to
104 tion, mineralization, and gene expression in cementoblasts using similar pathways while differentiall
105 ation of SMA9-labeled cells into osteoblasts/cementoblasts, we utilized a Col2.3GFP transgene, while
106 rine primary follicle cells and immortalized cementoblasts were delivered to the defects via biodegra
109 DGF-A may delay mineral formation induced by cementoblasts, while PDGF is clearly required for minera