Establishment and characterization of rat dental epithelial derived ameloblast-lineage clones

Abe, Kaori; Miyoshi, Keiko; Muto, Taro; Ruspita, Intan; Horiguchi, Taigo; Nagata, Toshihiko; Noma, Takafumi

doi:10.1263/jbb.103.479

Cited by 28 publications

(30 citation statements)

References 44 publications

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“…Next, we investigated Sp6 target genes with the combined methods of gain of function analysis and microarray analysis. We established an Sp6-overproducing clone, CHA9, which was transformed by Sp6 expression plasmid using ameloblast-lineage clone, G5 (11). CHA9 cells grow relatively much faster than control cells, which is consistent with previous reports on the cloning of Sp6 (3).…”

Section: Discussionsupporting

confidence: 87%

“…Sp6-stable transformants were established using an ameloblast-lineage clone, G5, as described previously (11). G5 cells were plated in 100 mm culture dishes and maintained in Dulbecco's modified Eagle's medium (DMEM)/Ham's F12 medium (Nissui, Tokyo, Japan) with 10% fetal bovine serum (FBS ; JRH Biosciences, Lenexa, KS).…”

Section: Establishment Of Sp6-stable Transformantsmentioning

confidence: 99%

“…Scale bar indicates 100 μm. lineage cell line, G5 (11). More than 100 clones were selected by G418 and established.…”

Section: Establishment Of An Sp6-overproducing Clone Cha9mentioning

confidence: 99%

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Sp6 downregulation of follistatin gene expression in ameloblasts

et al. 2008

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: Sp6 is a member of the Sp family of transcription factors that regulate a wide range of cellular functions, such as cell growth and differentiation. Sp6, also called epiprofin, is specifically expressed in tooth germ, limb bud, and hair follicle, but there is little information on its function.To investigate the possible role of Sp6 in tooth development, first we established an Sp6-overproducing clone, CHA9, and analyzed the features of the cell, including cell proliferation and gene expression. The parental cells of CHA9 are the ameloblast-lineage G5 cells that we previously established from rat dental epithelia of lower incisor. Sp6 overproduction accelerated cell proliferation and induced the expression of ameloblastin mRNA, a marker of ameloblast differentiation. Second, we performed genome-wide screening of Sp6 target genes by microarray analysis. Out of a total 20,450 genes, 448 genes were up-regulated and 500 genes were down-regulated by Sp6. We found the expression of follistatin, a BMP antagonist, to be 22.4-fold lower in CHA9 than in control cells. Transfection of the Sp6-antisense construct into CHA9 cells restored follistatin expression back to equivalent levels seen in control cells, indicating that Sp6 regulates follistatin gene expression in ameloblasts.Our findings demonstrate that the follistatin gene is one of the Sp6 target genes in ameloblasts and suggest that Sp6 promotes amelogenesis through inhibition of follistatin gene expression. J. Med. Invest. 55 : 87-98, February, 2008

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Section: Discussionsupporting

confidence: 87%

Section: Establishment Of Sp6-stable Transformantsmentioning

confidence: 99%

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Sp6 downregulation of follistatin gene expression in ameloblasts

et al. 2008

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“…Rat dental epithelia-derived cells, G5 (11) and its Sp6-stable transformant, C9 (3), were cultured in a Dulbecco's modified Eagle's medium and Ham's F12 medium (D/F12, Nissui, Tokyo, Japan) supplemented with 10% fetal bovine serum (FBS ; JRH Biosciences, Lenexa, KS, USA) incubated at 37! !…”

Section: Cell Culturementioning

confidence: 99%

Sp6 regulation of <i>Rock1 </i>promoter activity in dental epithelial cells

et al. 2014

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“…Previous studies suggest that dental epithelial stem cells and ameloblasts of incisors are regulated by a complex signaling network involving activin, BMP, FGF, notch, follistatin, and mitogen-activated protein kinase (MAPK) signaling that mediates the communication between mesenchymal and epithelial cells (Abe et al 2007;Harada et al 2002a, b;Wang et al 2007;Yokohama-Tamaki et al 2006). The MAPK family is conserved in evolution and is involved in diverse cellular processes such as cell growth and proliferation, and survival, innate immunity, and development among these signaling (Bogoyevitch and Court 2004;Ray et al 2007).…”

Section: Introductionmentioning

confidence: 99%

MAPK mediates Hsp25 signaling in incisor development

Lee

Cai

Kwak

et al. 2009

Histochem Cell Biol

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Rodent incisors are continuously growing teeth that include all stages of amelogenesis. Understanding amelogenesis requires investigations of the genes and their gene products control the ameloblast phenotype. One of the mechanisms related to tooth differentiation is mitogen-activated protein kinase (MAPK) signaling. The extracellular-signal regulated kinase (ERK)/mitogen-activated protein kinase kinase (MEK) cascade is associated with mechanisms that control the cell cycle and cell survival. However, the roles of cascades in incisor development remain to be determined. In this study, we investigated incisor development and growth in the mouse based on MAPK signaling. Moreover, heat-shock protein (Hsp)-25 is well known to be a useful marker of odontoblast differentiation. We used anisomycin (a protein-synthesis inhibitor that activates MAPKs) and U0126 (a MAPK inhibitor that blocks ERK1/2 phosphorylation) to examine the role of MAPKs in Hsp25 signaling in the development of the mouse incisor. We performed immunohistochemistry and in vitro culture using incisor tooth germ, and found that phospho-ERK (pERK), pMEK, and Hsp25 localized in developing incisor ameloblasts and anisomycin failed to produce incisor development. In addition, Western blotting results showed that anisomycin stimulated the phosphorylation of ERK, MEK, and Hsp25, and that some of these proteins were blocked by the U0126. These findings suggest that MAPK signals play important roles in incisor formation, differentiation, and development by mediating Hsp25 signaling.

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Establishment and characterization of rat dental epithelial derived ameloblast-lineage clones

Cited by 28 publications

References 44 publications

Sp6 downregulation of follistatin gene expression in ameloblasts

Sp6 downregulation of follistatin gene expression in ameloblasts

Sp6 regulation of <i>Rock1 </i>promoter activity in dental epithelial cells

MAPK mediates Hsp25 signaling in incisor development

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