| Autor: |
Kaligin, Maxim, Valijonov, Khojiakbar, Pliushkina, Aleksandra, Andreeva, Dina, Titova, Angelina, Titova, Marina, Ursan, Roman, Kiyasov, Andrey |
| Zdroj: |
BioNanoScience; Dec2022, Vol. 12 Issue 4, p1388-1393, 6p |
| Abstrakt: |
Postnatal islets of Langerhans retain cellular elements that have a several stem cell markers. It can be supposed that islet cells are not a static population and they can give rise to the new endocrinocytes. The aim of our work was to study the proliferative capacity of pancreatic islet cells and their subsequent differentiation in the late prenatal, early postnatal, and adult periods of human ontogenesis. A study of the late perinatal development of the human pancreas was performed on a sample resulting of legal medical abortion with the voluntary consent of the mother (30 weeks gestation), autopsy of the infant pancreas (from 17 days to 2 months after the birth) and adult pancreas (38–66 years old). Pancreas paraffin sections were stained immunohistochemically with commercial antibodies to insulin, Ki-67 (marker of proliferation), glucagon, and C-kit (stem and progenitor cell marker). It was found that proliferating cells remain in human pancreatic islets up to at least 2 months after the birth, the number of which can be up to 3.5% of islet cells. Some of these cells can synthesize glucagon. Based on the obtained results, we suppose that the cells of Langerhans islet are not a constant or static cells population. After the birth, there are cells in the islet which are capable to proliferate and differentiate. Because endocrinocyte differentiation into β-cells goes through the stage of glucagon-producing cells, it is possible that the origin of diabetes mellitus type I may be associated with the disturbance of proliferation and differentiation of the islet of Langerhans cells and a population imbalance between already differentiated α and β-cells. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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