Talk:Head Development: Difference between revisions
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http://www.ncbi.nlm.nih.gov/pubmed/18339367 | http://www.ncbi.nlm.nih.gov/pubmed/18339367 | ||
==2007== | |||
===Signaling by bone morphogenetic proteins directs formation of an ectodermal signaling center that regulates craniofacial development=== | |||
Dev Biol. 2007 Dec 1;312(1):103-14. Epub 2007 Sep 20. | |||
Foppiano S, Hu D, Marcucio RS. | |||
Department of Orthopaedic Surgery, San Francisco General Hospital, The University of California at San Francisco, School of Medicine, San Francisco, CA 94110, USA. | |||
Abstract | |||
We previously described a signaling center, the Frontonasal Ectodermal Zone (FEZ) that regulates growth and patterning of the frontonasal process (FNP). The FEZ is comprised of FNP ectoderm flanking a boundary between Sonic hedgehog (Shh) and Fibroblast growth factor 8 (Fgf8) expression domains. Our objective was to examine BMP signaling during formation of the FEZ. We blocked BMP signaling throughout the FNP prior to FEZ formation by infecting chick embryos at stage 10 (HH10) with a replication-competent avian retrovirus encoding the BMP antagonist Noggin. We assessed gene expression patterns in the FNP 72 h after infection (approximately HH22) and observed that Shh expression was reduced or absent. In the mesenchyme, we observed that Bmp2 transcripts were absent while the Bmp4 expression domain was expanded proximally. In addition to the molecular changes, infected embryos also exhibited facial malformations at 72 and 96 h after infection suggesting that the FEZ did not form. Our data indicate that reduced cell proliferation, but not apoptosis, in the mesenchyme contributed to the phenotype that we observed. Additionally, adding exogenous SHH into the mesenchyme of RCAS-Noggin-infected embryos did not restore Bmp2 and Bmp4 to a normal pattern of expression. These data indicate that BMP signaling mediates interactions between tissues in the FNP that regulate FEZ formation; and that the correct pattern of Bmp2 and Bmp4, but not Bmp7, expression in the FNP mesenchyme requires signaling by the BMP pathway. | |||
PMID: 18028903 | |||
===The development of Meckel's cartilage in staged human embryos during the 5th week=== | ===The development of Meckel's cartilage in staged human embryos during the 5th week=== | ||
Revision as of 15:10, 21 October 2010
2010
The Meckel's cartilage in human embryonic and early fetal periods
Anat Sci Int. 2010 Aug 27.
Wyganowska-Świątkowska M, Przystańska A.
Department of Conservative Dentistry and Periodontology, Poznan University of Medical Sciences, 70 Bukowska Street, 60-812, Poznan, Poland, marzena.wyganowska@periona.pl. Abstract The Meckel's cartilage itself and the mandible are derived from the first branchial arch, and their development depends upon the contribution of the cranial neural crest cells. The prenatal development of the Meckel's cartilage, along with its relationship to the developing mandible and the related structures, were studied histologically in human embryos and fetuses. The material was obtained from a collection of the Department of Anatomy, and laboratory procedures were used to prepare sections, which were stained according to standard light-microscopy methods. The formation of the Meckel's cartilage and its related structures was observed and documented. Some critical moments in the development of the Meckel's cartilage are suggested. The sequential development of the Meckel's cartilage started as early as stage 13 (32 days) with the appearance of condensation of mesenchymal cells within the mandibular prominence. During stage 17 (41 days), the primary ossification center of the mandible appeared on the inferior margin of the Meckel's cartilage. The muscular attachments to the Meckel's cartilage in embryos were observed at stage 18 (44 days). Their subsequent movement into the developing mandible during the 10th week seemed to diminish the role of the Meckel's cartilage as the supportive core; simultaneously, the process of regression within the cartilage was induced. During the embryonic period, the bilateral Meckel's cartilages were in closest contact at the posterior surface of their superior margins, preceding formation of the symphyseal cartilage at this site. The event sequence in the development of the Meckel's cartilage is finally discussed.
PMID: 20799009 http://www.ncbi.nlm.nih.gov/pubmed/20799009
Cells Tissues Organs. 2010 Sep 28. [Epub ahead of print]
Incidence and Development of the Human Supracochlear Cartilage.
Mérida Velasco JR, Rodríguez Vázquez JF, de la Cuadra Blanco C, Sanz Casado JV, Mérida Velasco JA.
Departamento de Anatomía y Embriología Humana II, Facultad de Medicina, Universidad Complutense de Madrid, Madrid, Spain. Abstract The supracochlear cartilage is known as an accessory cartilage of the chondrocranium situated between the otic capsule and the trigeminal ganglion. Although claimed to appear regularly during human development, its incidence and development have been reported only scarcely in the literature. The aim of this study was to describe the position and relationships of the supracochlear cartilage during its development. This study was made in 96 human specimens of 7-17 weeks of development, belonging to a collection of the Embryology Institute of Complutense University of Madrid. In addition, three-dimensional reconstruction of the supracochlear cartilage was made from 1 specimen. This cartilage, spherical in shape, appeared bilaterally in 23 specimens and unilaterally (left side) in 5. In our results, the supracochlear cartilage was found in 26.5% of the cases and was related to the trigeminal ganglion, the dura mater of the trigeminal cavity and the otic capsule. In 4 specimens, bilaterally, the supracochlear cartilage was continuous with the otic capsule. This work suggests that, based on the structures to which the supracochlear cartilage is related, it could be derived from the cranial neural crest.
PMID: 20881354 http://www.ncbi.nlm.nih.gov/pubmed/20881354
2009
The role of macrophages in the disappearance of Meckel's cartilage during mandibular development in mice
Tsuzurahara F, Soeta S, Kawawa T, Baba K, Nakamura M. Acta Histochem. 2009 Oct 22. [Epub ahead of print] PMID: 19853894
2008
Roles of FGFR3 during morphogenesis of Meckel's cartilage and mandibular bones
Havens BA, Velonis D, Kronenberg MS, Lichtler AC, Oliver B, Mina M. Dev Biol. 2008 Apr 15;316(2):336-49. Epub 2008 Feb 13.
To address the functions of FGFR2 and FGFR3 signaling during mandibular skeletogenesis, we over-expressed in the developing chick mandible, replication-competent retroviruses carrying truncated FGFR2c or FGFR3c that function as dominant negative receptors (RCAS-dnFGFR2 and RCAS-dnFGFR3). Injection of RCAS-dnFGFR3 between HH15 and 20 led to reduced proliferation, increased apoptosis, and decreased differentiation of chondroblasts in Meckel's cartilage. These changes resulted in the formation of a hypoplastic mandibular process and truncated Meckel's cartilage. This treatment also affected the proliferation and survival of osteoprogenitor cells in osteogenic condensations, leading to the absence of five mandibular bones on the injected side. Injection of RCAS-dnFGFR2 between HH15 and 20 or RCAS-dnFGFR3 at HH26 did not affect the morphogenesis of Meckel's cartilage but resulted in truncations of the mandibular bones. RCAS-dnFGFR3 affected the proliferation and survival of the cells within the periosteum and osteoblasts. Together these results demonstrate that FGFR3 signaling is required for the elongation of Meckel's cartilage and FGFR2 and FGFR3 have roles during intramembranous ossification of mandibular bones.
PMID: 18339367 http://www.ncbi.nlm.nih.gov/pubmed/18339367
2007
Signaling by bone morphogenetic proteins directs formation of an ectodermal signaling center that regulates craniofacial development
Dev Biol. 2007 Dec 1;312(1):103-14. Epub 2007 Sep 20.
Foppiano S, Hu D, Marcucio RS.
Department of Orthopaedic Surgery, San Francisco General Hospital, The University of California at San Francisco, School of Medicine, San Francisco, CA 94110, USA.
Abstract We previously described a signaling center, the Frontonasal Ectodermal Zone (FEZ) that regulates growth and patterning of the frontonasal process (FNP). The FEZ is comprised of FNP ectoderm flanking a boundary between Sonic hedgehog (Shh) and Fibroblast growth factor 8 (Fgf8) expression domains. Our objective was to examine BMP signaling during formation of the FEZ. We blocked BMP signaling throughout the FNP prior to FEZ formation by infecting chick embryos at stage 10 (HH10) with a replication-competent avian retrovirus encoding the BMP antagonist Noggin. We assessed gene expression patterns in the FNP 72 h after infection (approximately HH22) and observed that Shh expression was reduced or absent. In the mesenchyme, we observed that Bmp2 transcripts were absent while the Bmp4 expression domain was expanded proximally. In addition to the molecular changes, infected embryos also exhibited facial malformations at 72 and 96 h after infection suggesting that the FEZ did not form. Our data indicate that reduced cell proliferation, but not apoptosis, in the mesenchyme contributed to the phenotype that we observed. Additionally, adding exogenous SHH into the mesenchyme of RCAS-Noggin-infected embryos did not restore Bmp2 and Bmp4 to a normal pattern of expression. These data indicate that BMP signaling mediates interactions between tissues in the FNP that regulate FEZ formation; and that the correct pattern of Bmp2 and Bmp4, but not Bmp7, expression in the FNP mesenchyme requires signaling by the BMP pathway.
PMID: 18028903
The development of Meckel's cartilage in staged human embryos during the 5th week
Folia Morphol (Warsz). 2005 Feb;64(1):23-8.
Lorentowicz-Zagalak M, Przystańska A, Woźniak W. Department of Anatomy, University School of Medical Sciences, 60-781 Poznán, Poland.
Abstract The study was conducted on 15 embryos aged 5 weeks. The primordium of Meckel's cartilage appears at stage 13 (32 days) as a rounded structure composed of fusiform and polygonal cells, which blend with other cells of the mandibular process. At stages 14 and 15 (33 and 36 days) Meckel's cartilage forms a well delineated core of small densely packed cells.
PMID: 15832266