Peribiliary glands (PBGs) are clusters of epithelial cells residing in the submucosal compartment of extrahepatic bile ducts (EHBDs). While their function is largely undefined, they may represent a stem cell niche. Here, we hypothesized that PBGs are populated by mature and undifferentiated cells capable of proliferation in pathological states. To address this hypothesis, we developed a novel whole-mount immunostaining assay that preserves the anatomical integrity of EHBDs coupled with confocal microscopy, and found that PBGs populate the entire length of the extrahepatic biliary tract, except the gallbladder. Notably, in addition to the typical position of PBGs adjacent to the duct mucosa, PBGs elongate and form intricate intramural epithelial networks that communicate between different segments of the bile duct mucosa. Network formation begins where the cystic duct combines with hepatic ducts to form the common bile duct, and continues along the common bile duct. The cells of PBGs and the peribiliary network stain positively for α-tubulin, mucins, and chromogranin A, as well as for endoderm transcription factors Sox17 and Pdx1, and proliferate robustly following duct injury induced by virus infection and bile duct ligation.
Conclusion
PBGs form elaborate epithelial networks within the walls of EHBDs, contain cells of mature and immature phenotypes, and proliferate in response to bile duct injury. The anatomical organization of the epithelial network in tubules and the link with PBGs support an expanded cellular reservoir with the potential to restore the integrity and function of the bile duct mucosa in diseased states.
This chapter presents a study characterizing changes in carbohydrate moieties in the dorsal horn of the spinal cord of mice intoxicated with perivitellin 2 (PV2) from Pomacea canaliculata using lectin-histochemical techniques. Groups of 6 BALBcAnN mice were injected intraperitoneally with a single dose of PBS (control group) or 1 mg/kg PV2 (19 µg per mouse), and then their spinal cords were removed and lectin histochemistry was performed. The labelling of positively-stained lectins involved different areas of the spinal cord; nevertheless, comparisons between control and intoxicated animals showed that the most significant changes were detected in the grey matter with SBA (Glycine max) lectin. This lectin is a galactose-binding lectin that binds to oligosaccharide structures in which the terminal residue is derived from galactose or N-acetylgalactosamine. Thus, SBA-lectin neuronal staining which were moderately positive in laminae II and III of the grey matter of the spinal cord in control animals was strongly positive in the intoxicated animals. The rest of the lectins, despite showing different staining patterns in the grey matter, did not show any remarkable differences between control and intoxicated mice. UEA-1 (Ulex europaeus-1) lectin was the only one which displayed negative results for both control and inoculated animals. This study enhances current knowledge on the action of PV2 in the spinal cord of mice providing data on the lectin histochemical staining patterns.
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