Abstract
Mammalian esophagus exhibits a remarkable change in epithelial structure during the transition from embryo to adult. However, the molecular mechanisms of esophageal epithelial development are not well understood. Zebrafish (Danio rerio), a common model organism for vertebrate development and gene function, has not previously been characterized as a model system for esophageal epithelial development. In this study, we characterized a piece of non-keratinized stratified squamous epithelium similar to human esophageal epithelium in the upper digestive tract of developing zebrafish. Under the microscope, this piece was detectable at 5dpf and became stratified at 7dpf. Expression of esophageal epithelial marker genes (Krt5, P63, Sox2 and Pax9) was detected by immunohistochemistry and in situ hybridization. Knockdown of P63, a gene known to be critical for esophageal epithelium, disrupted the development of this epithelium. With this model system, we found that Pax9 knockdown resulted in loss or disorganization of the squamous epithelium, as well as down-regulation of the differentiation markers Krt4 and Krt5. In summary, we characterized a region of stratified squamous epithelium in the zebrafish upper digestive tract which can be used for functional studies of candidate genes involved in esophageal epithelial biology.
Highlights
The epithelial cells lining the human esophagus transform from simple columnar into ciliated epithelium at an early phase
Hematoxylin and eosin (H&E) staining on paraffin sections of the whole zebrafish showed the digestive tract was thoroughly lined with simple columnar cells, except for a small piece of non-keratinized stratified squamous epithelium on the dorsal side of the upper digestive tract
Our study demonstrates there is a stratified squamous epithelium located on the dorsal side of zebrafish upper digestive tract between the pharynx and the intestinal bulb
Summary
The epithelial cells lining the human esophagus transform from simple columnar into ciliated epithelium at an early phase. The ciliated epithelium is gradually replaced by squamous epithelium until a non-keratinized stratified squamous epithelium forms [1]. Morphological changes during human esophageal development have been well characterized for several decades, the molecular mechanisms underlying this process are not fully understood [2]. Some of the genes and pathways critical for esophageal development, such as P63, Sox, Nanog, Shh signaling and BMP signaling, are known to be important in esophageal diseases [3,4,5,6]. P63 regulates growth, invasion and metastasis of esophageal squamous cell carcinoma (ESCC) cells [7], and Sox functions as an amplified lineage-survival oncogene in PLOS ONE | DOI:10.1371/journal.pone.0143878. P63 regulates growth, invasion and metastasis of esophageal squamous cell carcinoma (ESCC) cells [7], and Sox functions as an amplified lineage-survival oncogene in PLOS ONE | DOI:10.1371/journal.pone.0143878 December 2, 2015
Sign-in/Register to view highlights & summary 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.
