Altered gene expression in rat cranial neural crest cells exposed to a teratogenic glucose concentration in vitro-paradoxical downregulation of antioxidative defense genes

Author(s):  
Parri Wentzel ◽  
Ulf J. Eriksson
2009 ◽  
Vol 1305 ◽  
pp. S50-S60 ◽  
Author(s):  
Parri Wentzel ◽  
Ulf J. Eriksson

2019 ◽  
Vol 86 ◽  
pp. 76-85 ◽  
Author(s):  
Partha Mukhopadhyay ◽  
Ratnam S. Seelan ◽  
Robert M. Greene ◽  
M. Michele Pisano

2018 ◽  
Author(s):  
Ayano Odashima ◽  
Shoko Onodera ◽  
Akiko Saito ◽  
Takashi Nakamura ◽  
Yuuki Ogihara ◽  
...  

AbstractCranial neural crest cells (cNCCs) comprise a multipotent population of cells that migrate into the pharyngeal arches of the vertebrate embryo and differentiate into a broad range of derivatives of the craniofacial organs. Consequently, migrating cNCCs are considered as one of the most attractive candidate sources of cells for regenerative medicine. In this study, we analyzed the gene expression profiles of cNCCs at different time points after induction by conducting three independent RNA sequencing experiments. We successfully induced cNCC formation from mouse induced pluripotent stem (miPS) cells by culturing them in neural crest inducing media for 14 days. We found that these cNCCs expressed several neural crest specifier genes but were lacking some previously reported specifiers, such as paired box 3 (Pax3), msh homeobox 1 (Msx1), and Forkhead box D3 (FoxD3), which are presumed to be essential for neural crest development in the embryo. Thus, a distinct molecular network may the control gene expression in miPS-derived cNCCs. We also found that c-Myc, ETS proto-oncogene 1, transcription factor (Ets1), and sex determining region Y-box 10 (Sox10) were only detected at 14 days after induction. Therefore, we assume that these genes would be useful markers for migratory cNCCs induced from miPS cells. Eventually, these cNCCs comprised a broad spectrum of protocadherin (Pcdh) and a disintegrin and metalloproteinase with thrombospondin motifs (Adamts) family proteins, which may be crucial in their migration.


Development ◽  
2001 ◽  
Vol 128 (11) ◽  
pp. 2143-2152 ◽  
Author(s):  
Sanjukta Sarkar ◽  
Anita Petiot ◽  
Andrew Copp ◽  
Patrizia Ferretti ◽  
Peter Thorogood

The cranial neural crest gives rise to most of the skeletal tissues of the skull. Matrix-mediated tissue interactions have been implicated in the skeletogenic differentiation of crest cells, but little is known of the role that growth factors might play in this process. The discovery that mutations in fibroblast growth factor receptors (FGFRs) cause the major craniosynostosis syndromes implicates FGF-mediated signalling in the skeletogenic differentiation of the cranial neural crest. We now show that, in vitro, mesencephalic neural crest cells respond to exogenous FGF2 in a dose-dependent manner, with 0.1 and 1 ng/ml causing enhanced proliferation, and 10 ng/ml inducing cartilage differentiation. In longer-term cultures, both endochondral and membrane bone are formed. FGFR1, FGFR2 and FGFR3 are all detectable by immunohistochemistry in the mesencephalic region, with particularly intense expression at the apices of the neural folds from which the neural crest arises. FGFRs are also expressed by subpopulations of neural crest cells in culture. Collectively, these findings suggest that FGFs are involved in the skeletogenic differentiation of the cranial neural crest.


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