In vitro studies on skeletogenic potential of membrane bone periosteal cells

Development ◽  
1979 ◽  
Vol 54 (1) ◽  
pp. 185-207
Author(s):  
Peter Thorogood

In the avian embryo ectomesenchyme cells, derived from the mesencephalic level of the cranial neural crest, migrate into the presumptive maxillary region and subsequently differentiateinto the membrane bones and associated secondary cartilage of the upper jaw skeleton. The cartilage arises secondarily within the periosteum at points of articulation between membrane bones and provides an embryonic articulating surface. The stimulus for the differentiation of secondary cartilage is believed to be intermittent pressure and shear created at the developing embryonic movement. The development of one such system - the quadratojugal, has been analysed using organ and explant culture techniques and studied with particular reference to the differentiation of periosteal cells into secondary cartilage. A number of conclusions were reached. (1) Normally only cells at discrete loci express a chondrogenic potential ,in vivo: the periosteal cells at these sites of future articulation become committed to chondrogenesis during stage 35, more than 24 h before cartilage is identifiable ,in vivo. (2) However, cells with a ‘latent’ chondrogenic potential are widespread in membrane bone periosteum and occur over most, if not all, of the surface area of the bone. This potential is expressed in the ‘permissive’ environment created by submersion of the tissue in explant culture or in submerged organ culture. (3) This chondrogenic potential exists long before the time at which commitment of cartilage-forming cells occurs and even presumptive maxillary ectomesenchyme at stage 29 has a limited ability to form cartilage ,in vitro. It is suggested that spatial position is a principal factor controlling the differentiation of secondary cartilage. Ectomesenchyme cells with the potential to form secondary cartilage are widespread but it is only those cells whose migration from the neural crest positions them and their progeny at the site of a presumptive joint which subsequently express this potential. This epigenetic interpretation is discussed in the general context of development mechanisms underlying the spatial and temporal patterns in which neural crest-derived cells differentiate to produce bone and cartilage during the formation of the head skeleton.

1993 ◽  
Vol 159 (1) ◽  
pp. 24-49 ◽  
Author(s):  
Nicole M. Le Douarin ◽  
Catherine Ziller ◽  
Gérard F. Couly

2021 ◽  
Vol 12 (6) ◽  
Author(s):  
Manuel Pedro Jimenez-García ◽  
Antonio Lucena-Cacace ◽  
Daniel Otero-Albiol ◽  
Amancio Carnero

AbstractThe EMX (Empty Spiracles Homeobox) genes EMX1 and EMX2 are two homeodomain gene members of the EMX family of transcription factors involved in the regulation of various biological processes, such as cell proliferation, migration, and differentiation, during brain development and neural crest migration. They play a role in the specification of positional identity, the proliferation of neural stem cells, and the differentiation of certain neuronal cell phenotypes. In general, they act as transcription factors in early embryogenesis and neuroembryogenesis from metazoans to higher vertebrates. The EMX1 and EMX2’s potential as tumor suppressor genes has been suggested in some cancers. Our work showed that EMX1/EMX2 act as tumor suppressors in sarcomas by repressing the activity of stem cell regulatory genes (OCT4, SOX2, KLF4, MYC, NANOG, NES, and PROM1). EMX protein downregulation, therefore, induced the malignance and stemness of cells both in vitro and in vivo. In murine knockout (KO) models lacking Emx genes, 3MC-induced sarcomas were more aggressive and infiltrative, had a greater capacity for tumor self-renewal, and had higher stem cell gene expression and nestin expression than those in wild-type models. These results showing that EMX genes acted as stemness regulators were reproduced in different subtypes of sarcoma. Therefore, it is possible that the EMX genes could have a generalized behavior regulating proliferation of neural crest-derived progenitors. Together, these results indicate that the EMX1 and EMX2 genes negatively regulate these tumor-altering populations or cancer stem cells, acting as tumor suppressors in sarcoma.


2013 ◽  
Vol 203 (4) ◽  
pp. 673-689 ◽  
Author(s):  
Ah-Lai Law ◽  
Anne Vehlow ◽  
Maria Kotini ◽  
Lauren Dodgson ◽  
Daniel Soong ◽  
...  

Cell migration is essential for development, but its deregulation causes metastasis. The Scar/WAVE complex is absolutely required for lamellipodia and is a key effector in cell migration, but its regulation in vivo is enigmatic. Lamellipodin (Lpd) controls lamellipodium formation through an unknown mechanism. Here, we report that Lpd directly binds active Rac, which regulates a direct interaction between Lpd and the Scar/WAVE complex via Abi. Consequently, Lpd controls lamellipodium size, cell migration speed, and persistence via Scar/WAVE in vitro. Moreover, Lpd knockout mice display defective pigmentation because fewer migrating neural crest-derived melanoblasts reach their target during development. Consistently, Lpd regulates mesenchymal neural crest cell migration cell autonomously in Xenopus laevis via the Scar/WAVE complex. Further, Lpd’s Drosophila melanogaster orthologue Pico binds Scar, and both regulate collective epithelial border cell migration. Pico also controls directed cell protrusions of border cell clusters in a Scar-dependent manner. Taken together, Lpd is an essential, evolutionary conserved regulator of the Scar/WAVE complex during cell migration in vivo.


1987 ◽  
Vol 104 (5) ◽  
pp. 1361-1374 ◽  
Author(s):  
J L Duband ◽  
S Dufour ◽  
K Hatta ◽  
M Takeichi ◽  
G M Edelman ◽  
...  

In avian embryos, somites constitute the morphological unit of the metameric pattern. Somites are epithelia formed from a mesenchyme, the segmental plate, and are subsequently reorganized into dermatome, myotome, and sclerotome. In this study, we used somitogenesis as a basis to examine tissue remodeling during early vertebrate morphogenesis. Particular emphasis was put on the distribution and possible complementary roles of adhesion-promoting molecules, neural cell adhesion molecule (N-CAM), N-cadherin, fibronectin, and laminin. Both segmental plate and somitic cells exhibited in vitro calcium-dependent and calcium-independent systems of cell aggregation that could be inhibited respectively by anti-N-cadherin and anti-N-CAM antibodies. In vivo, the spatio-temporal expression of N-cadherin was closely associated with both the formation and local disruption of the somites. In contrast, changes in the prevalence of N-CAM did not strictly accompany the remodeling of the somitic epithelium into dermamyotome and sclerotome. It was also observed that fibronectin and laminin were reorganized secondarily in the extracellular spaces after CAM-mediated contacts were modulated. In an in vitro culture system of somites, N-cadherin was lost on individual cells released from somite explants and was reexpressed when these cells reached confluence and established intercellular contacts. In an assay of tissue dissociation in vitro, antibodies to N-cadherin or medium devoid of calcium strongly and reversibly dissociated explants of segmental plates and somites. Antibodies to N-CAM exhibited a smaller disrupting effect only on segmental plate explants. In contrast, antibodies to fibronectin and laminin did not perturb the cohesion of cells within the explants. These results emphasize the possible role of cell surface modulation of CAMs during the formation and remodeling of some transient embryonic epithelia. It is suggested that N-cadherin plays a major role in the control of tissue remodeling, a process in which N-CAM is also involved but to a lesser extent. The substratum adhesion molecules, fibronectin and laminin, do not appear to play a primary role in the regulation of these processes but may participate in cell positioning and in the stabilization of the epithelial structures.


1997 ◽  
Vol 110 (14) ◽  
pp. 1673-1682 ◽  
Author(s):  
J.G. Stone ◽  
L.I. Spirling ◽  
M.K. Richardson

The peptide endothelin 3 (EDN3) is essential for normal neural crest development in vivo, and is a potent mitogen for quail truncal crest cells in vitro. It is not known which subpopulations of crest cells are targets for this response, although it has been suggested that EDN3 is selective for melanoblasts. In the absence of cell markers for different precursor types in the quail crest, we have characterised EDN3-responsive cell types using in vitro colony assay and clonal analysis. Colonies were analysed for the presence of Schwann cells, melanocytes, adrenergic cells or sensory-like cells. We provide for the first time a description of the temporal pattern of lineage segregation in neural crest cultures. In the absence of exogenous EDN3, crest cells proliferate and then differentiate. Colony assay indicates that in these differentiated cultures few undifferentiated precursors remain and there is a low replating efficiency. By contrast, in the presence of 100 ng/ml EDN3 differentiation is inhibited and most of the cells maintain the ability to give rise to mixed colonies and clones containing neural crest derivatives. A high replating efficiency is maintained. In secondary culture there was a progressive decline in the number of cell types per colony in control medium. This loss of developmental potential was not seen when exogenous EDN3 was present. Cell type analysis suggests two novel cellular targets for EDN3 under these conditions. Contrary to expectations, one is a multipotent precursor whose descendants include melanocytes, adrenergic cells and sensory-like cells; the other can give rise to melanocytes and Schwann cells. Our data do not support previous claims that the action of EDN3 in neural crest culture is selective for cells in the melanocyte lineage.


2006 ◽  
Vol 198 (2) ◽  
pp. 438-449 ◽  
Author(s):  
Jorge B. Aquino ◽  
Jens Hjerling-Leffler ◽  
Martin Koltzenburg ◽  
Thomas Edlund ◽  
Marcelo J. Villar ◽  
...  

2020 ◽  
Author(s):  
Alexander Goikoetxea ◽  
Erin L Damsteegt ◽  
Erica V Todd ◽  
Andrew McNaughton ◽  
Neil J Gemmell ◽  
...  

AbstractMany teleost fishes undergo natural sex change, and elucidating the physiological and molecular controls of this process offers unique opportunities not only to develop methods of controlling sex in aquaculture settings, but to better understand vertebrate sexual development more broadly. Induction of sex change in some sequentially hermaphroditic or gonochoristic fish can be achieved in vivo through social manipulation, inhibition of aromatase activity, and steroid treatment. However, the induction of sex change in vitro has been largely unexplored. In this study, we established an in vitro culture system for ovarian explants in serum-free medium for a model sequential hermaphrodite, the New Zealand spotty wrasse (Notolabrus celidotus). This culture technique enabled evaluating the effect of various treatments with 17β-estradiol (E2), 11-ketotestosterone (11KT) or cortisol (CORT) on spotty wrasse ovarian architecture for 21 days. A quantitative approach to measuring the degree of ovarian atresia within histological images was also developed, using pixel-based machine learning software. Ovarian atresia likely due to culture was observed across all treatments including no-hormone controls, but was minimised with treatment of at least 10 ng/mL E2. Neither 11KT nor CORT administration induced proliferation of spermatogonia (i.e. sex change) in the cultured ovaries indicating culture beyond 21 days may be needed to induce sex change in vitro. The in vitro gonadal culture and analysis systems established here enable future studies investigating the paracrine role of sex steroids, glucocorticoids and a variety of other factors during gonadal sex change in fish.


1991 ◽  
Vol 58 (4) ◽  
pp. 401-409 ◽  
Author(s):  
Thomas J. Hayden ◽  
Denise Brennan ◽  
Katherine Quirke ◽  
Paddie Murphy

SummaryXanthine oxidase/dehydrogenase (XO/XDH) increases at mid gestation in mammary gland but not in liver of the mouse and remains elevated until the pups are weaned at 20 d post partum. The increase in enzyme activity is due neither to alteration in activators or inhibitors nor to a production of a variant enzyme with altered catalytic properties. The increase is preceded in vivo by a surge of prolactin-like activity (placental lactogen) in plasma, and prolactin is required for induction of XO/XDH in explant culture in vitro. Induction of XO/XDH in vivo and in vitro precedes the full histological differentiation of the gland. In addition, induction of XO/XDH in vitro occurs more rapidly and at lower concentrations of prolactin than does histological differentiation. Thus although XO/XDH is present in milk, increased XO/XDH activity is an early event in mammogenesis in vivo and in vitro rather than a terminal component of differentiation.


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