Cranial neural crest cell contribution to craniofacial formation, pathology, and future directions in tissue engineering

Snider, Taylor Nicholas; Mishina, Yuji

doi:10.1002/bdrc.21075

Cited by 39 publications

(35 citation statements)

References 49 publications

(56 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…During and after migration, these cells contribute to the development of most of the craniofacial structures, generating, based on the effect of specific genetic and epigenetic factors and according to a hierarchical model of lineage segregation, a very wide range of ectomesenchymal and neural derivatives [33,34,35,36,37,38,39,40,41,42,43,44]. Several syndromes and congenital conditions termed neurocristopathies, which include, among others, DiGeorge syndrome, Waardenburg syndrome, and craniofacial microsomia, are well known to be related to reduced survival and improper migration of these cells [45,46,47]. Specifical- …”

Section: Discussionmentioning

confidence: 99%

Glial choristoma of the tongue. Clinicopathological analysis of a case and pathogenetic insights

Corsi¹,

Veccia²,

Riminucci³

2017

pjp

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

Glial choristoma of the tongue. Clinicopathological analysis of a case and pathogenetic insights

Corsi¹,

Veccia²,

Riminucci³

2017

pjp

View full text Add to dashboard Cite

“…It is well known that the neural crest cells (NCCs) are required for proper craniofacial development and they contribute to the formation of most viscerocranium structures such as frontonasal process and teeth, while the posterior parts of viscerocranium are from mesoderm (29, 30). In the current study, abnormal craniofacial bone morphology is consistently associated with Evc2 expression patterns.…”

Section: Discussionmentioning

confidence: 99%

Expression of Evc2 in craniofacial tissues and craniofacial bone defects in Evc2 knockout mouse

Badri

Zhang

Ohyama

et al. 2016

Archives of Oral Biology

Self Cite

View full text Add to dashboard Cite

Objective Our objectives were to determine the expression of EVC2 in craniofacial tissues and investigate the effect of Evc2 deficiency on craniofacial bones using Evc2 knockout (KO) mouse model. Design Evc2 KO mice were generated by introducing a premature stop codon followed by the Internal Ribosomal Entry Site fused to β-galactosidase (LacZ). Samples from wild-type (WT), heterozygous (Het) and homozygous Evc2 KO mice were prepared. LacZ staining and immunohistochemistry (IHC) with anti-β-galactosidase, anti-EVC2 and anti-SOX9 antibodies were performed. The craniofacial bones were stained with alcian blue and alizarin red. Results The LacZ activity in KO was mainly observed in the anterior parts of viscerocranium. The Evc2-expressing cells were identified in many cartilageous regions by IHC with anti-β-galactosidase antibody in KO and Het embryos. The endogenous EVC2 protein was observed in these areas in WT embryos. Double labeling with anti-SOX9 antibody showed that these cells were mainly chondrocytes. At adult stages, the expression of EVC2 was found in chondrocytes of nasal bones and spheno-occipital synchondrosis, and osteocytes and endothelial-like cells of the premaxilla and mandible. The skeletal double staining demonstrated that craniofacial bones, where the expression of EVC2 was observed, in KO had the morphological defects as compared to WT. Conclusion To our knowledge, our study was the first to identify the types of Evc2-expressing cells in craniofacial tissues. Consistent with the expression pattern, abnormal craniofacial bone morphology was found in the Evc2 KO mice, suggesting that EVC2 may be important during craniofacial growth and development.

show abstract

“…Individual genes within these pathways have been implicated in the etiology of CS, both in humans and animal models [Snider and Mishina, 2014]. Interestingly, most of these pathways are known to play pivotal roles in neural crest development, hence driving the morphogenesis of the craniofacial complex [Twigg and Wilkie, 2015b; Mishina and Snider, 2014].…”

Section: Genetic Etiopathogenesis Of Craniosynostosismentioning

confidence: 99%

Genetic advances in craniosynostosis

Lattanzi

Barba

Pietro

et al. 2017

American J of Med Genetics Pt A

View full text Add to dashboard Cite

Craniosynostosis, the premature ossification of one or more skull sutures, is a clinically and genetically heterogeneous congenital anomaly affecting approximately 1 in 2,500 live births. In most cases, it occurs as an isolated congenital anomaly, i.e. nonsyndromic craniosynostosis (NCS), the genetic and environmental causes of which remain largely unknown. Recent data suggest that at least some of the midline NCS cases may be explained by two loci inheritance. In approximately 25–30% of patients craniosynostosis presents as a feature of a genetic syndrome due to chromosomal defects or mutations in genes within interconnected signaling pathways. The aim of this review is to provide a detailed and comprehensive update on the genetic and environmental factors associated with NCS, integrating the scientific findings achieved during the last decade. Focus on the neurodevelopmental, imaging and treatment aspects of NCS is also provided.

show abstract

Cranial neural crest cell contribution to craniofacial formation, pathology, and future directions in tissue engineering

Cited by 39 publications

References 49 publications

Glial choristoma of the tongue. Clinicopathological analysis of a case and pathogenetic insights

Glial choristoma of the tongue. Clinicopathological analysis of a case and pathogenetic insights

Expression of Evc2 in craniofacial tissues and craniofacial bone defects in Evc2 knockout mouse

Genetic advances in craniosynostosis

Contact Info

Product

Resources

About