Reduced differentiation of intestinal epithelial cells in wasting marmoset syndrome
| Autor: | Eiki Takahashi, Kimie Niimi |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
Pathology
medicine.medical_specialty endocrine system animal structures Cellular differentiation Enteroendocrine cell digestive system common marmoset Jejunum Laboratory Animal Science biology.animal medicine Animals Intestinal Mucosa Lamina propria General Veterinary biology Full Paper Wasting Syndrome Marmoset intestinal epithelial cell Callithrix Cell Differentiation Epithelial Cells differentiation biology.organism_classification Intestines Mononuclear cell infiltration wasting marmoset syndrome medicine.anatomical_structure Stem cell |
| Zdroj: | The Journal of Veterinary Medical Science |
| ISSN: | 1347-7439 0916-7250 |
| Popis: | Wasting marmoset syndrome (WMS) is a serious disease in captive common marmoset (Callithrix jacchus) colonies. Because of the high mortality rates, elucidation of the underlying mechanisms is essential. In this study, we compared the histopathology, the number of each epithelial cell in the jejunum and colon, and the expression patterns of some molecular markers between healthy and WMS-affected marmosets. Atrophy of villi in the jejunum and mononuclear cell infiltration in the lamina propria were observed in the intestinal tract of WMS-affected marmosets. Although the numbers of transient amplifying cells and tuft cells were increased, the number of goblet cells was obviously decreased in the jejunum and colon of WMS-affected marmosets compared to healthy marmosets. In addition, the number of enterocytes in the jejunum was decreased in WMS animals. There was no apparent difference in the numbers of stem cells, enteroendocrine cells, or Paneth cells. The expression of β-catenin and Tcf7l2 was increased in WMS, and the co-existence of β-catenin and Tcf7l2/Cyclin D1 was observed around the crypts in WMS-affected marmosets. These findings suggest that cell proliferation continues, but cell differentiation is halted in the intestinal tract due to the enhanced β-catenin/Tcf7l2/Cyclin D1signaling pathway in WMS, which results in malfunction of the villus and mucosa. |
| Databáze: | OpenAIRE |
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