Abstract
A recent study from our lab revealed that the inhibition of cyclooxygenase-2 (COX-2) exclusively reduces the level of PGE2 (Prostaglandin E2) among prostanoids and hampers the normal development of several structures, strikingly the cranial vault, in chick embryos. In order to unearth the mechanism behind the deviant development of cranial features, the expression pattern of various factors that are known to influence cranial neural crest cell (CNCC) migration was checked in chick embryos after inhibiting COX-2 activity using etoricoxib. The compromised level of cell adhesion molecules and their upstream regulators, namely CDH1 (E-cadherin), CDH2 (N-cadherin), MSX1 (Msh homeobox 1), and TGF-β (Transforming growth factor beta), observed in the etoricoxib-treated embryos indicate that COX-2, through its downstream effector PGE2, regulates the expression of these factors perhaps to aid the migration of CNCCs. The histological features and levels of FoxD3 (Forkhead box D3), as well as PCNA (Proliferating cell nuclear antigen), further consolidate the role of COX-2 in the migration and survival of CNCCs in developing embryos. The results of the current study indicate that COX-2 plays a pivotal role in orchestrating craniofacial structures perhaps by modulating CNCC proliferation and migration during the embryonic development of chicks.
Highlights
Introductioncranial neural crest cell (CNCC) are clusters of multipotent cells and fate-restricted progenitors that can differentiate into a multitude of tissue types based on the molecular signals they receive [3]
Craniofacial development involves the formation of cranial neural crest cells (CNCCs) via epithelial–mesenchymal transition (EMT), induction, delamination, and migration, followed by the morphogenesis of various organs of an organism [1]
A significant decrease in COX-2 activity was recorded in the treated embryos during the early developmental stages, namely Hamburger–Hamilton stage 6 (Day-1), HH 12 (Day-2), and HH 20 (Day-3), known for EMT and CNCC migration, respectively, compared to the control group (Figure 1)
Summary
CNCCs are clusters of multipotent cells and fate-restricted progenitors that can differentiate into a multitude of tissue types based on the molecular signals they receive [3]. Their precursors undergo EMT and migrate from the forebrain, midbrain, and rhombomeres of the hindbrain to populate at the pharyngeal arches and contribute to the patterning of head and face structures. Once CNCCs pass through the EMT process, they begin migration. During migration, they proliferate and increase the pool of cells
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
