Role of Tenascin in Cancer Development
Róza Ádány in Tumor Matrix Biology, 2017
The neural crest is a population of transient cells that migrate from the dorsal neural tube along defined pathways to numerous locations in embryos. During migration, neural crest cells proliferate and differentiate into a variety of cell types, including neurons, accessory cells of the peripheral nervous system, melanocytes, neurosecretory cells, and mesenchymal cells. The ECM is probably very important in determining the direction of neural crest cell migration. In amphibian, avian, and mammalian embryos, tenascin and fibronectin have been demonstrated along the pathways of neural crest cells by immunohistochemistry. Tenascin codistributes with migrating cells, whereas fibronectin is more widespread. Therefore, it can be speculated that fibronectin provides the substrate while tenascin paves the way for cell migration. In support of this speculation, in vitro observations have revealed that the migration rate of neural crest cells from neural tube expiants was greater on tenascin-coated plastic than fibronectin-coated plastic.78 Other investigators, however, have shown that tenascin/cytotactin in the substrate inhibits neural crest cell migration on fibronectin.79
New Aspects of Isotretinoin Teratogenicity
Ayse Serap Karadag, Berna Aksoy, Lawrence Charles Parish in Retinoids in Dermatology, 2019
Initiation of craniofacial morphogenesis is marked by the appearance of the paired pharyngeal arches. The first pair is divided into mandibular and maxillary prominences, which together with the frontonasal prominence constitute the five facial primordia. The neural crest arises from the embryonic ectoderm and develops from the neural tube after its closure (11). The neural crest is a stem/progenitor cell population that contributes to a wide variety of derivatives, including sensory and autonomic ganglia, cartilage and bone of the face, and pigment cells of the skin (12). Cranial NCCs are stem cell-line cells, which delaminate from the dorsal edge of the developing brain and drive the budding of the five primordia (13–15). In NCCs, NCC-derived neuroblastoma cells as well as sebocytes, isotretinoin is intracellularly isomerized to all-trans-retinoic acid (ATRA) (4,8,16,17).
Formation of the Cranial Base and Craniofacial Joints
D. Dixon Andrew, A.N. Hoyte David, Ronning Olli in Fundamentals of Craniofacial Growth, 2017
The neural crest of vertebrate embryos is a temporary structure that develops from the lateral ridges of the neural plate at the time of neural tube closure, progressing incrementally in a craniocaudal direction along the entire length of the neural tube. It is important in the present context to take note of an important distinction between trunk and head neural crest. Much of the trunk crest is used for building up parts of the nervous system, such as the spinal ganglia, the trunk musculature, and a considerable contribution to connective tissue formation, including the sheaths of muscles and tendons (Hamilton et al., 1964; Moore, 1993). However, trunk crest cells do not differentiate into cartilage (Hörstadius, 1950). Instead, most of the head crest is used to form the anterior part of the chondrocranium, the cartilaginous forerunner of the skull base, and almost all of the cartilaginous visceral arch skeleton, as well as membrane-bone osteogenesis in the craniofacial region.
Glia: from ‘just glue’ to essential players in complex nervous systems: a comparative view from flies to mammals
Published in Journal of Neurogenetics, 2018
Maria Losada-Perez
The PNS glia is originated in the neural crest. Similar to the CNS, neural crest cells first give rise to neurons (sensory neurons of the dorsal root ganglia) before generating glia. This precursor cells generate the Swchann cells precursors and the Satellite glia which remains in PNS ganglia and ensheathes the neuronal cells bodies to metabolically support neurons (Huang, Gu, & Chen, 2013). Schwann cells precursors migrate to the peripheral nerves where they differentiate into either myelinating or non-myelinating Schwann cells. Moreover, neural crest cells also generate the enteric glia, present in the intestinal tract (Coelho-Aguiar Jde et al., 2015) and, at least, part of the olfactory ensheathing cells (OECs) (Barraud et al., 2010; Forni et al., 2011).
The Notch pathway: a novel therapeutic target for cardiovascular diseases?
Published in Expert Opinion on Therapeutic Targets, 2019
Giorgio Aquila, Aleksandra Kostina, Francesco Vieceli Dalla Sega, Eugeniy Shlyakhto, Anna Kostareva, Luisa Marracino, Roberto Ferrari, Paola Rizzo, Anna Malaschicheva
A recent study of a cohort of 428 patients with a spectrum of diseases affecting aortic development such as aortic valve stenosis, a bicuspid aortic valve, aortic valve insufficiency coarctation of the aorta, and hypoplastic left heart syndrome, subvalvular or supravalvular aortic stenosis, hypoplastic aortic arch, interruption of the aorta, and mitral valve anomalies clearly demonstrates that the phenotypic spectrum of NOTCH1 mutations includes a wide variety of pathologies affecting the whole conotruncus of the heart [45]. This is in agreement with the described role of the Notch pathway in determining the fate of neural crest–derived cells. Alagille syndrome (ALGS), a congenital disease that mainly affects liver ducts and heart development, in the vast majority (up to 96%) of patients, is caused by mutations in JAGGED1 and NOTCH2 (in 1–2% of the cases) [46].
Review and perspective of tissue engineering therapy for the treatment of corneal endothelial decompensation
Published in Expert Review of Ophthalmology, 2020
Naoki Okumura, Noriko Koizumi
Our view of the next five years is that one or more cellular therapy products for the treatment of endothelial decompensation will be approved for clinical use. Careful randomized studies of the effectiveness and safety of tissue engineering therapies in comparison to DMEK, long time follow-up studies, and medical cost analyses are also anticipated once a cellular therapy product is introduced. In addition, several approaches for producing CECs or CEC-like cells from pluripotent stem cells, such as embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs), have been reported [68697071–72]. Most of the protocols induce CECs following the induction of neural crest cells, thereby mimicking the developmental process [73]. Further establishment of the protocol is needed to guarantee the function and safety; however, transplantation of induced CECs derived from pluripotent stem cells might come to clinical trial in the future. We have entered an exciting era when we might experience a paradigm shift wherein a common therapy such as keratoplasty will be replaced with a novel tissue engineering therapy.