Site‐specific function and regulation of Osterix in tooth root formation

He, Yueqiu; Sui, Bing‐Dong; Li, M.; Huang, Jinghui; Chen, S.; Wu, Li-An

doi:10.1111/iej.12585

Cited by 24 publications

(28 citation statements)

References 54 publications

(134 reference statements)

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“…Later at postnatal stages, when the root is already developed but still elongating, Runx2 expression declines while Osx expression continues to be present in the alveolar bone and in the dental pulp. 20 These findings would account for the results in the present study, in which Osx expression was identified in the osteoblast cells of the alveolar bone and in the odontoblast cells of the pulp dentinal zone of the molar teeth of the posterior samples of the mandibles treated with all decalcification methods. Interestingly, within the same samples, no Runx2 expression was visible regardless of decalcification treatment.…”

Section: Discussionsupporting

confidence: 81%

Comparison of Different Decalcification Methods Using Rat Mandibles as a Model

Savi

Brierly

Baldwin

et al. 2017

J Histochem Cytochem.

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Selection of decalcification agents is an essential consideration when processing mineralized tissues because the integrity and immunohistochemical characteristics of the tissues may be affected. Here, we report results obtained from the decalcification of rat mandibles using 10% ethylenediaminetetraacetic acid (EDTA) at room temperature (RT), 10% EDTA at 37C, 5% nitric acid, and 10% formic acid at RT. Decalcification endpoints were determined by microcomputed tomography. Morphological preservation and antigenicity were evaluated by hematoxylin and eosin staining and immunohistochemistry. Decalcification of the anterior and posterior portions of the mandible took 220 and 191 hr in 10% EDTA RT, 102 and 73 hr in 10% EDTA 37C, 13.5 and 4.3 hr in 5% nitric acid, and 140 and 36 hr in 10% formic acid, respectively. Decalcification in 10% EDTA at 37C was accelerated, but 10% EDTA at RT provided optimal results for immunohistochemistry and cellular and structural details. Decalcification using 5% nitric acid was accomplished in the shortest time and exhibited good cellular and architectural morphology, whereas 10% formic acid was suboptimal with respect to tissue and cellular morphology. Despite being the slowest method, EDTA at RT is still the recommended method for decalcifying mineralized tissues; however, if rapid decalcification is needed, 5% nitric acid is the best option, yielding acceptable tissue integrity and speed.

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Section: Discussionsupporting

confidence: 81%

Comparison of Different Decalcification Methods Using Rat Mandibles as a Model

Savi

Brierly

Baldwin

et al. 2017

J Histochem Cytochem.

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“…This suggests that Osx contributes to MD regression. Osx has wellestablished roles in osteoblast, odontoblast, and cementoblast differentiation (16,24). However, this is evidence for Osx function in sex differentiation.…”

Section: Transcriptome Analysis Identifies Candidate Genes Up-regulatmentioning

confidence: 99%

Osterixfunctions downstream of anti-Müllerian hormone signaling to regulate Müllerian duct regression

Mullen

Wang

Liu

et al. 2018

Proc. Natl. Acad. Sci. U.S.A.

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In mammals, the developing reproductive tract primordium of male and female fetuses consists of the Wolffian duct and the Müllerian duct (MD), two epithelial tube pairs surrounded by mesenchyme. During male development, mesenchyme-epithelia interactions mediate MD regression to prevent its development into a uterus, oviduct, and upper vagina. It is well established that transforming growth factor-β family member anti-Müllerian hormone (AMH) secreted from the fetal testis and its type 1 and 2 receptors expressed in MD mesenchyme regulate MD regression. However, little is known about the molecular network regulating downstream actions of AMH signaling. To identify potential AMH-induced genes and regulatory networks controlling MD regression in a global nonbiased manner, we examined transcriptome differences in MD mesenchyme between males (AMH signaling on) and females (AMH signaling off) by RNA-seq analysis of purified fetal MD mesenchymal cells. This analysis found 82 genes up-regulated in males during MD regression and identified ()/, a key transcriptional regulator of osteoblast differentiation and bone formation, as a downstream effector of AMH signaling during MD regression. /OSX was expressed in a male-specific pattern in MD mesenchyme during MD regression. OSX expression was lost in mutant males without AMH signaling. In addition, transgenic mice ectopically expressing human AMH in females induced a male pattern of expression. Together, these results indicate that AMH signaling is necessary and sufficient for expression in the MD mesenchyme. In addition, MD regression was delayed in-null males, identifying as a factor that regulates MD regression.

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“…This suggests that Osx contributes to MD regression. Osx has well-established roles in osteoblast, odontoblasts, and cementoblasts differentiation (16,24). However, this is the first evidence for Osx function in sex differentiation.…”

Section: Regression Is Delayed In Osx Null Male Micementioning

confidence: 76%