The proliferating field of neural crest stem cells

Abstract

Neural crest stem cells were first isolated from early embryonic neural crest in the early 1990s, but in the past 5 years, there has been a burst of discoveries of neural crest-derived stem cells from diverse locations. Here, we summarize these data, highlighting the characteristics of each stem cell type. These cells vary widely in the markers they express and the variety of cell types they appear to generate. They occupy diverse locations, but in some cases multiple stem cell types apparently occupy physically proximate niches. To date, few molecular similarities can be identified between these stem cells, although a systematic comparison is required. We note other issues worthy of attention, including aspects of the in vivo behavior of these stem cells, their niches, and their lineage relationships. Together, analysis of these issues will clarify this expanding, but still young, field and contribute to exploration of the important therapeutic potential of these cells. Developmental Dynamics 236:3242-3254, 2007.

<b>Induction of neural crest cells from human dental pulp-derived induced pluripotent stem </b><b>cells </b>

“…Further analyses are required to examine the differences between iPS cell-derived and ES cell-derived NCCs in terms of CD73 expression. We next tested whether the migrated cells had the potential to differentiate into multi-lineage neural crest derivatives, such as osteoblasts, chondrocytes, and Schwann cells, by in vitro and in vivo assays (9). As a preliminary experiment, the osteogenic differentiation potential of the migrated cells was tested by directly switching to osteogenic induction medi- um from neural induction medium at 80% confluency, however the migrated cells did not exhibit osteogenic differentiation potential.…”

Isolation and Characterization of Neural Crest Stem Cells Derived From In Vitro–Differentiated Human Embryonic Stem Cells

“…It gives rise to a vast array of histologically and geographically diverse cell types including, among others, skeletal cells, myofibroblasts, melanocytes, and nearly all the cells of the peripheral nervous system including sympathetic and parasympathetic ganglia, the adrenal medulla, autonomic and sensory neurons, and supporting glial cells (i.e., Schwann and satellite) (reviewed in ref. 1). Given the diversity of its progeny, it is not surprising that disruption of the neural crest adversely affects human development and several complex human disorders such as DiGeorge, Waardenburg and Apert syndromes, neurofibromatosis, and Hirschsprung's disease arise because of aberrations in neural crest development [2,3].…”

“…Multipotent NCSCs then respond to differentiation and migration signals and undergo progressive fate restrictions, giving rise to progenitor cells (NCPCs) with varying degrees of self-renewal and differentiation potential that are determined by both cell autonomous as well as environmental factors (reviewed in ref. [1]). …”

“…Thus, the feasibility of acquiring primary human neural crest cells from embryonic tissue is severely challenged by both ethical and technical issues-in fact, neural crest induction and migration is underway long before most women even realize that they are pregnant. Although NCSCs have been isolated from some human adult tissues, they are exceedingly rare and do not possess the same selfrenewal and pluripotency of early embryonic NCSCs [1,11,12]. Therefore, to fully advance in vitro studies of human neural crest development alternate renewable sources of precursor cells will be required.…”

Protein tyrosine phosphatase activity in the neural crest is essential for normal heart and skull development

“…NCCs are first localized in the neural folds at the dorsal aspect of the developing spinal cord and delaminate from the neural tube. They then migrate via different pathways toward the organ primordia, where they give rise to and influence the development of a diverse array of tissues, including numerous craniofacial structures, the cardiac outflow tract (OFT), the endocrine glands, and neurons (10). Therefore, some of the defects observed in NCFC syndromes may arise principally from perturbation of NCC determination, proliferation, migration, or differentiation.…”