Wnt-RhoA signaling is involved in dental enamel development.

Wnt-RhoA signaling is involved in dental enamel development.
复制标题

DOI:
10.1111/j.1600-0722.2011.00880.x
复制
发表时间:
2011-12
影响因子:
1.9
通讯作者:
Gibson CW
Gibson CW
中科院分区:
医学4区
文献类型:
--
作者:
Peng L;Li Y;Shusterman K;Kuehl M;Gibson CW

文献摘要

参考文献

被引文献

相似文献

在成釉细胞中表达显性失活 RhoA (RhoADN) 的转基因小鼠具有发育不全的牙釉质,并存在磨牙尖缺陷。 RhoADN转基因小鼠牙釉质器官中β-catenin和Wnt5a表达上调,这表明经典和非经典Wnt通路均参与釉质缺陷形成过程。据推测,成釉细胞中表达的 RhoADN 通过氟化物诱导的途径干扰正常牙釉质发育。在氟化物处理的成釉细胞系细胞系 (ALC) 中进一步研究了 Wnt 和 RhoA 通路。 RhoA 和 ROCK II 的活性显着降低,与 RhoADN 转基因小鼠的活性相似。 NaF 处理后,经典和非经典 Wnt 通路均被激活,并通过 Western blot 和 TOPflash(β-catenin-TCF/LEF 报告基因)测定进行验证。在氟化物处理的 ALC 中,定位于细胞质和细胞核的 β-连环蛋白上调,而 Wnt 通路的负调节因子 Gsk-3β 则表现出表达模式下降。目前的结果表明,Wnt 和 RhoA 途径均与氟化物诱导的 ALC 信号转导以及 RhoADN 转基因小鼠牙釉质缺陷的发展有关。
Transgenic mice that express dominant negative RhoA (RhoADN) in ameloblasts have hypoplastic enamel, with defects in molar cusps. β-catenin and Wnt5a were up-regulated in enamel organs of RhoADN transgenic mice, which indicated that both canonical and non-canonical Wnt pathways were implicated in the process of enamel defect formation. It was hypothesized that RhoADN expressed in ameloblasts interfered with normal enamel development through the pathways that were induced by fluoride. The Wnt and RhoA pathways were further investigated in an ameloblast-lineage cell line (ALC) with treatment by fluoride. The activities of RhoA and ROCK II decreased significantly, similar to activities in RhoADN transgenic mice. Both the canonical and non-canonical Wnt pathways were activated by treatment of NaF, which were verified by Western blot and TOPflash (β-catenin-TCF/LEF reporter gene) assay. β-catenin localization to both cytoplasm and nucleus was up-regulated in fluoride treated ALC while Gsk-3β, the negative regulator of the Wnt pathway, showed a decreased expression pattern. The current results indicated that both Wnt and RhoA pathways are implicated in fluoride induced signaling transductions in ALC as well as the development of enamel defects in RhoADN transgenic mice.
DOI: 10.1128/mcb.24.10.4487-4501.2004
发表时间: 2004-05-01
影响因子: 5.3
作者:
Kishida, S;Yamamoto, H;Kikuchi, A
通讯作者: Kikuchi, A
DOI: 10.1016/s0960-9822(02)00864-3
发表时间: 2002-06-04
期刊: CURRENT BIOLOGY
影响因子: 9.2
作者:
Marlow, F;Topczewski, J;Solnica-Krezel, L
通讯作者: Solnica-Krezel, L
DOI: 10.1016/j.cellsig.2009.05.010
发表时间: 2009-11
影响因子: 4.8
作者:
Rossol-Allison J;Stemmle LN;Swenson-Fields KI;Kelly P;Fields PE;McCall SJ;Casey PJ;Fields TA
通讯作者: Fields TA
DOI: 10.1101/gad.230302
发表时间: 2002-05-01
影响因子: 10.5
作者:
Amit, S;Hatzubai, A;Alkalay, I
通讯作者: Alkalay, I
DOI: 10.1073/pnas.0607289103
发表时间: 2006-12-05
影响因子: 11.1
作者:
Jarvinen, Elina;Salazar-Ciudad, Isaac;Thesleff, Irma
通讯作者: Thesleff, Irma