Experiments showing the role of migrating neural crest (mesectoderm) in the formation of head skeleton and loose connective tissue in Rana palustris

1929 ◽  
Vol 118 (1) ◽  
pp. 40-77 ◽  
Author(s):  
L. S. Stone
Development ◽  
1988 ◽  
Vol 102 (2) ◽  
pp. 301-310 ◽  
Author(s):  
R.M. Langille ◽  
B.K. Hall

Lamprey embryos were obtained by artificial fertilization to ascertain the contributions made by the neural crest to the head skeleton. Early-neurula-stage embryos of Petromyzon marinus were subjected to neural crest extirpation along the anterior half from one of seven zones, raised to a larval stage at which control larvae exhibit well-developed skeletons and analysed by light microscopy for any abnormalities to the cranial and visceral skeleton. The removal of premigratory neural crest at the level of the anterior prosencephalon (zone I) and at the level of somites 6 to 8 (zone VII) had no effect on skeletal development. However, the extirpation of neural crest from the intervening regions was positively correlated with deletions/reductions to the trabeculae (basicranial elements) and to the branchial arches (viscerocranial elements). Alterations to the trabeculae (16/27 cases, or 59%) occurred only after extirpation of zones II-V (corresponding to the posterior prosencephalon to midrhombencephalon) while alterations to the branchial arches (21/28 cases, or 75%) occurred only after removal of neural crest from zones III-VI (corresponding to the mesencephalon to the level of the fifth somite). Furthermore, the first three branchial arches were correlated in a majority of cases with neural crest from zone III, the next two arches with zones IV, V and VI and the last two arches with zone VI. Organs that develop within or adjacent to the area of neural crest extirpation such as the brain, notochord and lateral mesodermal derivatives were not affected. Parachordals were never altered by the operations nor were there any discernible changes to developing mucocartilage or to the prechondrogenic otic capsule. The contributions of the neural crest to the petromyzonid head skeleton described herein are compared with the roles of neural crest in the development of cranial and visceral skeletal elements in other vertebrates. The importance of these findings to the current hypothesis of the phylogeny of the vertebrate skeleton and the central role of the neural crest in vertebrate cephalization is discussed.


Development ◽  
1984 ◽  
Vol 79 (1) ◽  
pp. 243-255
Author(s):  
Billie J. Swalla ◽  
Michael Solursh

This paper examines the differentiation of somites from stage-16 or -17 chick embryos cultured with or without notochord in explant cultures. Histological sections of the cultures were stained with a trichrome stain to identify the different kinds of connective tissues formed. Both anterior and posterior (epithelial) somites made muscle, cartilage and loose connective tissue in explant culture. The extent of cartilage differentiation was enhanced by the presence of the notochord, confirming earlier studies. The presence of 1 mM-dibutyryl cAMP in the culture medium increased the amount of muscle found in the explants but by histological criteria did not inhibit chondrogenesis, contrary to earlier reports. The addition of quail ectoderm to the explants stimulated loose connective tissue to form directly beneath it, suggesting for the first time a role of the ectoderm in dermatome differentiation. These results suggest that the epithelial somite has the capacity to differentiate into all three connective tissue types even before it has separated into sclerotome and dermamyotome. The relative amount of different connective tissue types can be influenced by environmental factors, such as adjacent epithelia like the notochord or ectoderm.


2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 1046.3-1047
Author(s):  
V. Pulito-Cueto ◽  
S. Remuzgo Martinez ◽  
F. Genre ◽  
B. Atienza-Mateo ◽  
V. M. Mora-Cuesta ◽  
...  

Background:Interstitial lung disease (ILD) is one of the most significant complications of connective tissue diseases (CTD), leading to an increase of the morbidity and mortality in patients with CTD [1]. A specific T cell subset termed angiogenic T cells (TAng), that promote endothelial repair and revascularization, have been involved in the pathogenesis of CTD [2-4]. However, to the best of our knowledge, no information regarding the role of TAng in CTD-ILD+ is available.Objectives:To study, for the first time, the potential role of TAng related to vascular damage in CTD-ILD+.Methods:Peripheral venous blood was collected from 40 patients with CTD-ILD+ and three comparative groups: 44 CTD-ILD- patients, 21 idiopathic pulmonary fibrosis (IPF) patients and 20 healthy controls (HC). All subjects were recruited from the Rheumatology and Pneumology departments of Hospital Universitario Marqués de Valdecilla, Santander, Spain. Quantification of TAng was performed by flow cytometry. TAng were considered as triple-positive for CD3, CD31 and CXCR4.Results:Patients with CTD-ILD+ exhibited a significantly lower TAng frequency than CTD-ILD- patients (p<0.001). Similar results were obtained when patients with CTD-ILD+ were compared with HC (p=0.004) although no difference was observed between CTD-ILD+ and IPF. In addition, a significant increase of TAng frequency was shown in patients with CTD-ILD- in relation to IPF patients (p<0.001), while no difference was observed between CTD-ILD- and HC.Conclusion:Our results reveal a decrease of TAng frequency related to vascular damage in CTD-ILD+. Furthermore, we disclose that the presence of ILD is associated with lower TAng frequency.References:[1]Expert Rev Clin Immunol 2018;14(1):69-82.[2]Circulation 2007;116(15):1671-82.[3]Ann Rheum Dis 2015 74(5):921-7.[4]PLoS One 2017;12(8):e0183102.Acknowledgements:Personal funds, VP-C: PREVAL18/01 (IDIVAL); SR-M: RD16/0012/0009 (ISCIII-ERDF); LL-G: INNVAL20/06 (IDIVAL); RP-F: START PROJECT (FOREUM); RL-M: Miguel Servet type I CP16/00033 (ISCIII-ESF).Disclosure of Interests:Verónica Pulito-Cueto: None declared, Sara Remuzgo Martinez: None declared, Fernanda Genre: None declared, Belén Atienza-Mateo: None declared, Victor Manuel Mora-Cuesta: None declared, David Iturbe-Fernández: None declared, Leticia Lera-Gómez: None declared, Raquel Pérez-Fernández: None declared, Pilar Alonso Lecue: None declared, Javier Rodriguez Carrio: None declared, Diana Prieto-Peña: None declared, Virginia Portilla: None declared, Ricardo Blanco Speakers bureau: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen and MSD, Consultant of: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen and MSD, Grant/research support from: Abbvie, MSD and Roche, Alfonso Corrales: None declared, Jose Manuel Cifrián-Martínez: None declared, Raquel López-Mejías: None declared, Miguel A González-Gay Speakers bureau: Pfizer, Abbvie, MSD, Grant/research support from: Pfizer, Abbvie, MSD


2021 ◽  
Vol 22 (14) ◽  
pp. 7299
Author(s):  
David M. Klyne ◽  
Mary F. Barbe ◽  
Greg James ◽  
Paul W. Hodges

Musculoskeletal conditions are known to involve biological, psychological, social and, often, lifestyle elements. However, these domains are generally considered in isolation from each other. This siloed approach is unlikely to be adequate to understand the complexity of these conditions and likely explains a major component of the disappointing effects of treatment. This paper presents a hypothesis that aims to provide a foundation to understand the interaction and integration between these domains. We propose a hypothesis that provides a plausible link between psychology and lifestyle factors with tissue level effects (such as connective tissue dysregulation/accumulation) in musculoskeletal conditions that is founded on understanding the molecular basis for interaction between systemic and local inflammation. The hypothesis provides plausible and testable links between mind and body, for which empirical evidence can be found for many aspects. We present this hypothesis from the perspective of connective tissue biology and pathology (fibrosis), the role of inflammation locally (tissue level), and how this inflammation is shaped by systemic inflammation through bidirectional pathways, and various psychological and lifestyle factors via their influence on systemic inflammation. This hypothesis provides a foundation for new consideration of the development and refinement of personalized multidimensional treatments for individuals with musculoskeletal conditions.


2006 ◽  
Vol 235 (10) ◽  
pp. 2722-2735 ◽  
Author(s):  
Binnur Eroglu ◽  
Guanghu Wang ◽  
Naxin Tu ◽  
Xutong Sun ◽  
Nahid F. Mivechi

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