Pluripotent stem cell transcription factors during human odontogenesis

Cunha, Juliana Malta da; Costa-Neves, Adriana; Kerkis, Irina; Silva, Marcelo Cavenaghi Pereira da

doi:10.1007/s00441-013-1658-y

Cited by 24 publications

(22 citation statements)

References 30 publications

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“…In the absence of PGD 2 , Nanog, Oct4 and Sox2 are ectopically expressed in mutant foetal testes and display cytoplasmic localisation, suggesting that PGD 2 might also participates in the nuclear translocation of these transcription factors as has been previously observed for Sox9 (Malki et al, 2005). This phenotype might reflect a transient and incomplete differentiation of the germline, as described in embryonic stem cells (da Cunha et al, 2013;Elatmani et al, 2011) and in a variety of cancer cells (Gu et al, 2012;Guo et al, 2011).…”

Section: Cip1mentioning

confidence: 53%

Prostaglandin D2 acts through the Dp2 receptor to influence male germ cell differentiation in the foetal mouse testis

et al. 2014

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Through intercellular signalling, the somatic compartment of the foetal testis is able to program primordial germ cells to undergo spermatogenesis. Fibroblast growth factor 9 and several members of the transforming growth factor β superfamily are involved in this process in the foetal testis, counteracting the induction of meiosis by retinoic acid and activating germinal mitotic arrest. Here, using in vitro and in vivo approaches, we show that prostaglandin D 2 (PGD 2 ), which is produced through both L-Pgds and H-Pgds enzymatic activities in the somatic and germ cell compartments of the foetal testis, plays a role in mitotic arrest in male germ cells by activating the expression and nuclear localization of the CDK inhibitor p21Cip1 and by repressing pluripotency markers. We show that PGD 2 acts through its Dp2 receptor, at least in part through direct effects in germ cells, and contributes to the proper differentiation of male germ cells through the upregulation of the master gene Nanos2. Our data identify PGD 2 signalling as an early pathway that acts in both paracrine and autocrine manners, and contributes to the differentiation of germ cells in the foetal testis.

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Section: Cip1mentioning

confidence: 53%

Prostaglandin D2 acts through the Dp2 receptor to influence male germ cell differentiation in the foetal mouse testis

et al. 2014

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“…In terms of pluripotency, Oct4 and Nanog play important roles in the proliferation and self-renewal of stem cells28. Previous reports have shown that Oct4 and Nanog are expressed in the dental epithelium and mesenchyme and regulate cell proliferation, stemness, and differentiation in stem cells4344. Nakagawa et al ., using tooth germ organ culture and Oct4 siRNA, also found that OCT4 was critical for tooth epithelial stem cell proliferation and self-renewal45.…”

Section: Discussionmentioning

confidence: 99%

Maternal diabetes modulates dental epithelial stem cells proliferation and self-renewal in offspring through apurinic/apyrimidinicendonuclease 1-mediated DNA methylation

Chen

Zhang

et al. 2017

Sci Rep

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Maternal gestational diabetes mellitus (GDM) has many adverse effects on the development of offspring. Aberrant DNA methylation is a potential mechanism associated with these effects. However, the effects of GDM on tooth development and the underlying mechanisms have not been thoroughly investigated. In the present study, a GDM rat model was established and incisor labial cervical loop tissue and dental epithelial stem cells (DESCs) were harvested from neonates of diabetic and control dams. GDM significantly suppressed incisor enamel formation and DESCs proliferation and self-renewal in offspring. Gene expression profiles showed that Apex1 was significantly downregulated in the offspring of diabetic dams. In vitro, gain and loss of function analyses showed that APEX1 was critical for DESCs proliferation and self-renewal and Oct4 and Nanog regulation via promoter methylation. In vivo, we confirmed that GDM resulted in significant downregulation of Oct4 and Nanog and hypermethylation of their promoters. Moreover, we found that APEX1 modulated DNA methylation by regulating DNMT1 expression through ERK and JNK signalling. In summary, our data suggest that GDM-induced APEX1 downregulation increased DNMT1 expression, thereby inhibiting Oct4 and Nanog expression, through promoter hypermethylation, resulting in suppression of DESCs proliferation and self-renewal, as well as enamel formation.

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“…Cell proliferation, fate and death are regulated by elements found in the niche [ 74 -76 ]. The interaction between transcription factors such as Oct-4, Sox-2, Nanog and Stat-3 results in stem cell niche formation [ 77 ]. By evaluating BrdU uptake of proliferating cells in the pulp tissue, DPSC niches were claimed to reside in perivascular regions [ 78 ].…”

Section: Dsc Nichesmentioning

confidence: 99%