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The role of Rho signaling pathway in dental epithelial stem cells
Keishi Otsu 1 , Ryota Kishigami 1 , Ai OikawaSasaki 1 , Naoki Fujiwara 1 ,
Kiyoto Ishizeki 1 , Hidemitsu Harada 1
1
Dept. Anatomy, Iwate Med. Univ., 2 Advanced Oral Health Science Research
Center, Iwate Med. Univ.
We have recently found that Rho signaling plays an important role in ameloblast
differentiation through maintenance of the cell polarity Otsu et al. Journal of
Cellular Physiology, 2010. Consequently, we next focused on the role of Rho
signaling in dental epithelial stem cells. In this study, we examined the function of
ROCK, downstream Rho effectors, in dental epithelial cells isolated from mouse
incisor apical bud. After treatment of ROCK inhibitor and knocking down ROCK
by siRNA, the shape of cells changed from epithelial phenotype to mesenchymal
like cells, and cellcell adhesions were lost. Real time RTPCR showed that
ROCK inhibitor decreased expression of epithelial cell markers, and increased
mesenchymal and stem cell markers. In the treated cells, mRNA expressions
of slug, which is epithelialmesenchymal transition markers, increased and the
intense nuclear accumulation was observed. In mouse incisor, slug was strongly
expressed in apical bud compared to differentiated ameloblasts. Based on the
data, we consider that Rhoslug signaling pathway is closely involved with the
maintenance of dental epithelial stem cells.
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Localization of osteopontin and osterix in periodontal tissue during
orthodontic tooth movement in rats
Ji Youn Kim, Byung In Kim, Seong Suk Jue, Jae Hyun Park, Je Won Shin
Department of Oral Anatomy, Graduate School of Dentistry, Kyung Hee
University, Seoul, KOREA
The aim of this study was to evaluate the localization of osteopontin OPN
and osterix in periodontal tissue during experimental tooth movement with
heavy force in rats. Nickeltitanium closedcoil springs were used to create a
100g mesial force to the maxillary first molars. On days 3, 7, 10, and 14 after
force application, histological changes in periodontal tissue were examined by
immunohistochemistry using proliferating cell nuclear antigen PCNA, OPN, and
osterix. PCNApositive cells were found close to the alveolar bone and cementum
on both sides. OPNpositive cells were observed along the cementing line of the
cementum and bone on both sides and also were visible along with newly formed
fibers in the periodontal ligament on the tension side. Osterixpositive cells were
strongly detected on the surface of the alveolar bone and cementum on both sides.
During tooth movement, periodontal remodeling occurs on both sides. These
results indicate that OPN and osterix may play an important role of differentiation
and osteoblasts and cementoblasts matrix formation during periodontal tissue
remodeling.
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Fetal jaw movement affects molecular cascade in the development of
mandibular condylar cartilage
Esrat Jahan 1,2 3 1 Ashiq Mahmood Rafiq 1,2
2 1
1
2
3
Fetal jaw movement restriction has been shown to cause deformity of the
mandibular condyle. We hypothesized that this treatment affects the expression
of mechanosensitive molecules, namely Indian hedgehog Ihh and bone
morphogenetic protein2 Bmp2 in the condyle. We restrained jaw movement
by suturing the jaw of E15.5 mouse embryos and allowed them to develop
until E18.5 using exo utero system. Morphological, histomorphometric and
immunohistochemical study showed that the mandibular condylar cartilage
was deformed, volume and total cell number were reduced, and number and/
or distribution of 5bromo2′deoxyuridinepositive cells, Ihh and Bmp2
positive cells in the mesenchymal and prehypertrophic zones were significantly
and correspondingly decreased in the sutured group. Our results revealed that
the mechanical stress induced by prenatal jaw movement restriction decreased
proliferating cells, the amount of cartilage, and altered expression of the Ihh and
Bmp2, suggesting that Ihh and Bmp2 act as mechanotransduction mediators in
the development of mandibular condylar cartilage.
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1 2
1
2
FGF18
Phase Field
P
1 1 1 2 3 1
1
2 3 I
Muscle
tendon junction: MTJMTJ
ArgGlyAsp
RGD
RGDserine S
MTJ
RGDS
ECM
RGDS
RGDS
RGDS
RGDS
MTJ
P
1 2 2 3 4
4 5 1 1
1
2
3
RI 4 5
19 4
ECM
iTRAQQ
NanoLC
MALDITOF/TOF MS/MS
core protein collagen GAG
Type I & II collagen GAGType I collagen
Type II collagen
ECM